<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <version>1.0</version>
  <creation_date>2009-07-21 20:27:02 UTC</creation_date>
  <update_date>2026-05-14 16:40:30 UTC</update_date>
  <accession>T3D2809</accession>
  <common_name>Oxycodone</common_name>
  <class>SmallMolecule</class>
  <description>Oxycodone belongs to the phenanthrenes and derivatives, a class of benzenoids within the organic compounds. This exogenous compound has the formula C18H21NO4 and an average molecular weight of 315.36 g/mol. At room temperature, it exists as a solid. It is used as an opioid analgesic, mu-opioid receptor agonist, analgesic, and antitussive (PMC7941040). It is used as a treatment for pain (PMC7012325) and chronic pain (PMC6205722), though it is associated with lethargy and depression (PMC7012325).

Oxycodone targets the mu-type opioid receptor (OPRM1), kappa-type opioid receptor (OPRK1), and delta-type opioid receptor (OPRD1), while also acting as an inhibitor of the voltage-dependent N-type calcium channel subunit alpha-1B (CACNA1B). Within the central nervous system (CNS), it acts as a weak agonist at the mu, kappa, and delta opioid receptors. It primarily affects mu-type opioid receptors, which are coupled with G-protein receptors and function as modulators of synaptic transmission via G-proteins that activate effector proteins. Binding stimulates the exchange of GTP for GDP on the G-protein complex. Because the effector system consists of cAMP and adenylate cyclase located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase.

Oxycodone is recorded in several sources, including analgesics, drinking water, the preparation of vinegar, and household cleaning and consumer products such as pipe accessories, other smoking requisites, and non-electric simulated smoking devices. It is also found in electrical and electronic equipment, including antennas, amplifiers, relays, auxiliary devices, and line transmission systems. Recorded exposure routes include oral and rectal administration.</description>
  <categories>
    <category>Drug</category>
    <category>Synthetic Toxin</category>
  </categories>
  <types>
    <type>Organic Compound</type>
    <type>Amine</type>
    <type>Ether</type>
    <type>Drug</type>
    <type>Analgesic, Opioid</type>
    <type>Narcotic</type>
    <type>Antitussive Agent</type>
    <type>Opiate Agonist</type>
    <type>Metabolite</type>
    <type>Synthetic Compound</type>
    <type>Human Neurotoxin</type>
  </types>
  <synonyms>
    <synonym>(-)-14-Hydroxydihydrocodeinone</synonym>
    <synonym>4,5-Epoxy-14-hydroxy-3-methoxy-17-methylmorphinan-6-one</synonym>
    <synonym>4,5alpha-Epoxy-14-hydroxy-3-methoxy-17-methylmorphinan-6-one</synonym>
    <synonym>Dihydro-14-hydroxycodeinone</synonym>
    <synonym>Dihydrohydroxycodeinone</synonym>
    <synonym>Dihydrohydroxycondeinone</synonym>
    <synonym>Dihydrone</synonym>
    <synonym>Dihydroxycodeinone</synonym>
    <synonym>Oxanest</synonym>
    <synonym>Oxecta</synonym>
    <synonym>Oxicodona</synonym>
    <synonym>Oxycodonum</synonym>
    <synonym>Oxycontin</synonym>
    <synonym>OxyIR</synonym>
    <synonym>PTI-821</synonym>
    <synonym>Roxicodone</synonym>
  </synonyms>
  <chemical_formula>C18H21NO4</chemical_formula>
  <average_molecular_weight>315.3636</average_molecular_weight>
  <monisotopic_moleculate_weight>315.147058165</monisotopic_moleculate_weight>
  <iupac_name>(1S,5R,13R,17S)-17-hydroxy-10-methoxy-4-methyl-12-oxa-4-azapentacyclo[9.6.1.0^{1,13}.0^{5,17}.0^{7,18}]octadeca-7(18),8,10-trien-14-one</iupac_name>
  <traditional_iupac>(1S,5R,13R,17S)-17-hydroxy-10-methoxy-4-methyl-12-oxa-4-azapentacyclo[9.6.1.0^{1,13}.0^{5,17}.0^{7,18}]octadeca-7(18),8,10-trien-14-one</traditional_iupac>
  <cas_registry_number>76-42-6</cas_registry_number>
  <smiles>[H][C@@]12OC3=C(OC)C=CC4=C3[C@@]11CCN(C)[C@]([H])(C4)[C@]1(O)CCC2=O</smiles>
  <inchi>InChI=1S/C18H21NO4/c1-19-8-7-17-14-10-3-4-12(22-2)15(14)23-16(17)11(20)5-6-18(17,21)13(19)9-10/h3-4,13,16,21H,5-9H2,1-2H3/t13-,16+,17+,18-/m1/s1</inchi>
  <inchikey>BRUQQQPBMZOVGD-XFKAJCMBSA-N</inchikey>
  <taxonomy>
    <kingdom>Organic compounds</kingdom>
    <super_class>Benzenoids</super_class>
    <class>Phenanthrenes and derivatives</class>
    <sub_class/>
    <direct_parent>Phenanthrenes and derivatives</direct_parent>
    <alternate_parents>
      <alternative_parent>1,2-aminoalcohols</alternative_parent>
      <alternative_parent>Alkyl aryl ethers</alternative_parent>
      <alternative_parent>Anisoles</alternative_parent>
      <alternative_parent>Aralkylamines</alternative_parent>
      <alternative_parent>Azacyclic compounds</alternative_parent>
      <alternative_parent>Coumarans</alternative_parent>
      <alternative_parent>Cyclic alcohols and derivatives</alternative_parent>
      <alternative_parent>Hydrocarbon derivatives</alternative_parent>
      <alternative_parent>Isoquinolones and derivatives</alternative_parent>
      <alternative_parent>Ketones</alternative_parent>
      <alternative_parent>Organic oxides</alternative_parent>
      <alternative_parent>Organopnictogen compounds</alternative_parent>
      <alternative_parent>Oxacyclic compounds</alternative_parent>
      <alternative_parent>Piperidines</alternative_parent>
      <alternative_parent>Tertiary alcohols</alternative_parent>
      <alternative_parent>Tetralins</alternative_parent>
      <alternative_parent>Trialkylamines</alternative_parent>
    </alternate_parents>
    <substituents>
      <substituent>1,2-aminoalcohol</substituent>
      <substituent>Alcohol</substituent>
      <substituent>Alkyl aryl ether</substituent>
      <substituent>Amine</substituent>
      <substituent>Anisole</substituent>
      <substituent>Aralkylamine</substituent>
      <substituent>Aromatic heteropolycyclic compound</substituent>
      <substituent>Azacycle</substituent>
      <substituent>Carbonyl group</substituent>
      <substituent>Coumaran</substituent>
      <substituent>Cyclic alcohol</substituent>
      <substituent>Ether</substituent>
      <substituent>Hydrocarbon derivative</substituent>
      <substituent>Isoquinolone</substituent>
      <substituent>Ketone</substituent>
      <substituent>Organic nitrogen compound</substituent>
      <substituent>Organic oxide</substituent>
      <substituent>Organic oxygen compound</substituent>
      <substituent>Organoheterocyclic compound</substituent>
      <substituent>Organonitrogen compound</substituent>
      <substituent>Organooxygen compound</substituent>
      <substituent>Organopnictogen compound</substituent>
      <substituent>Oxacycle</substituent>
      <substituent>Phenanthrene</substituent>
      <substituent>Piperidine</substituent>
      <substituent>Tertiary alcohol</substituent>
      <substituent>Tertiary aliphatic amine</substituent>
      <substituent>Tertiary amine</substituent>
      <substituent>Tetralin</substituent>
    </substituents>
    <molecular_framework>Aromatic heteropolycyclic compounds</molecular_framework>
    <descriptors>
      <descriptor>organic heteropentacyclic compound</descriptor>
    </descriptors>
  </taxonomy>
  <status>Detected and Not Quantified</status>
  <origin>Exogenous</origin>
  <cellular_locations>
    <cellular_location>Cytoplasm</cellular_location>
    <cellular_location>Extracellular</cellular_location>
    <cellular_location>Membrane</cellular_location>
  </cellular_locations>
  <biofluid_locations/>
  <tissue_locations/>
  <pathways>
    <pathway>
      <name>Oxycodone Action Pathway</name>
      <smpdb_id>SMP0000409</smpdb_id>
      <kegg_map_id/>
    </pathway>
    <pathway>
      <name>Oxycodone Opioid Agonist Action Pathway</name>
      <smpdb_id>SMP0125024</smpdb_id>
      <kegg_map_id/>
    </pathway>
    <pathway>
      <name>Oxycodone Drug Metabolism Action Pathway</name>
      <smpdb_id>SMP0142951</smpdb_id>
      <kegg_map_id/>
    </pathway>
    <pathway>
      <name>Oxycodone Predicted Metabolism Pathway</name>
      <smpdb_id>SMP0174781</smpdb_id>
      <kegg_map_id/>
    </pathway>
  </pathways>
  <state>Solid</state>
  <appearance>White powder.</appearance>
  <experimental_properties>
    <property>
      <kind>melting_point</kind>
      <value>219°C</value>
    </property>
    <property>
      <kind>solubility</kind>
      <value>100 mg/ml</value>
    </property>
    <property>
      <kind>logp</kind>
      <value>0.3</value>
    </property>
  </experimental_properties>
  <predicted_properties>
    <property>
      <kind>logp</kind>
      <value>1.04</value>
      <source>ALOGPS</source>
    </property>
    <property>
      <kind>logs</kind>
      <value>-1.75</value>
      <source>ALOGPS</source>
    </property>
    <property>
      <kind>solubility</kind>
      <value>5.59e+00 g/l</value>
      <source>ALOGPS</source>
    </property>
    <property>
      <kind>logp</kind>
      <value>1.03</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>pka_strongest_acidic</kind>
      <value>13.56</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>pka_strongest_basic</kind>
      <value>8.21</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>iupac</kind>
      <value>(1S,5R,13R,17S)-17-hydroxy-10-methoxy-4-methyl-12-oxa-4-azapentacyclo[9.6.1.0^{1,13}.0^{5,17}.0^{7,18}]octadeca-7(18),8,10-trien-14-one</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>average_mass</kind>
      <value>315.3636</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>mono_mass</kind>
      <value>315.147058165</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>smiles</kind>
      <value>[H][C@@]12OC3=C(OC)C=CC4=C3[C@@]11CCN(C)[C@]([H])(C4)[C@]1(O)CCC2=O</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>formula</kind>
      <value>C18H21NO4</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>inchi</kind>
      <value>InChI=1S/C18H21NO4/c1-19-8-7-17-14-10-3-4-12(22-2)15(14)23-16(17)11(20)5-6-18(17,21)13(19)9-10/h3-4,13,16,21H,5-9H2,1-2H3/t13-,16+,17+,18-/m1/s1</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>inchikey</kind>
      <value>BRUQQQPBMZOVGD-XFKAJCMBSA-N</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>polar_surface_area</kind>
      <value>59</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>refractivity</kind>
      <value>84.04</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>polarizability</kind>
      <value>32.79</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>rotatable_bond_count</kind>
      <value>1</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>acceptor_count</kind>
      <value>5</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>donor_count</kind>
      <value>1</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>physiological_charge</kind>
      <value>1</value>
      <source>ChemAxon</source>
    </property>
    <property>
      <kind>formal_charge</kind>
      <value>0</value>
      <source>ChemAxon</source>
    </property>
  </predicted_properties>
  <route_of_exposure>Oral; enteral (rectal).&#13;Well absorbed with an oral bioavailability of 60% to 87%</route_of_exposure>
  <mechanism_of_toxicity>Oxycodone acts as a weak agonist at mu, kappa, and delta opioid receptors within the central nervous system (CNS). Oxycodone primarily affects mu-type opioid receptors, which are coupled with G-protein receptors and function as modulators, both positive and negative, of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is inhibited. Opioids such as oxycodone also inhibit the release of vasopressin, somatostatin, insulin, and glucagon. Opioids close N-type voltage-operated calcium channels (kappa-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (mu and delta receptor agonist). This results in hyperpolarization and reduced neuronal excitability.</mechanism_of_toxicity>
  <metabolism>Hepatic&#13;Route of Elimination: Oxycodone and its metabolites are excreted primarily via the kidney.&#13;Half Life: 4.5 hours</metabolism>
  <toxicity/>
  <lethaldose/>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use_source>For the treatment of diarrhoea, pulmonary oedema and for the relief of moderate to moderately severe pain.</use_source>
  <min_risk_level/>
  <health_effects>#&lt;HealthEffect::ActiveRecord_Associations_CollectionProxy:0x00007f7265f0f0a8&gt;</health_effects>
  <symptoms>Symptoms of overdose include respiratory depression, somnolence progressing to stupor or coma, skeletal muscle flaccidity, cold and clammy skin, constricted pupils, bradycardia, hypotension, and death.</symptoms>
  <treatment>To treat Oxycodone overdose, primary attention should be given to the reestablishment of a patent airway and institution of assisted or controlled ventilation. Supportive measures (including oxygen and vasopressors) should be employed in the management of circulatory shock and pulmonary edema accompanying overdose as indicated. Cardiac arrest or arrhythmias may require cardiac massage or defibrillation. The narcotic antagonists, naloxone or nalmefene, are specific antidotes for opioid overdose. Opioid antagonists should not be administered in the absence of clinically significant respiratory or circulatory depression secondary to Oxycodone overdose. If needed the appropriate dose of naloxone hydrochloride or nalmefene should be administered simultaneously with efforts at respiratory resuscitation (see package insert for each drug for the details). Since the duration of action of oxycodone may exceed that of the antagonist, the patient should be kept under continued surveillance and repeated doses of the antagonist should be administered as needed to maintain adequate respiration. Gastric emptying may be useful in removing unabsorbed drug. (L1712)</treatment>
  <drugbank_id>DB00497</drugbank_id>
  <hmdb_id>HMDB14640</hmdb_id>
  <pubchem_compound_id>5284603</pubchem_compound_id>
  <chembl_id>CHEMBL656</chembl_id>
  <chemspider_id>4447649</chemspider_id>
  <kegg_id>C08018</kegg_id>
  <uniprot_id/>
  <omim_id/>
  <chebi_id>7852</chebi_id>
  <biocyc_id/>
  <ctd_id/>
  <stitch_id>Oxycodone</stitch_id>
  <actor_id/>
  <pdb_id/>
  <wikipidia>Oxycodone</wikipidia>
  <general_references>
    <reference>
      <pubmed_id>17525040</pubmed_id>
    </reference>
    <reference>
      <pubmed_id>18039433</pubmed_id>
    </reference>
    <reference>
      <reference_text>Drugs.com: http://www.drugs.com/cons/Oxycodone.html</reference_text>
    </reference>
    <reference>
      <reference_text>RxList: The Internet Drug Index (2009).: http://www.rxlist.com/</reference_text>
    </reference>
  </general_references>
  <targets>
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      <target_id/>
      <mechanism_of_action/>
      <constants/>
      <references/>
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    <target>
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      <constants/>
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      <constants/>
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      <constants/>
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      <constants/>
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      <constants/>
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      <target_id>BE0000632</target_id>
      <mechanism_of_action>Oxycodone acts as a weak agonist at mu, kappa, and delta opioid receptors within the central nervous system (CNS). Oxycodone primarily affects mu-type opioid receptors, which are coupled with G-protein receptors and function as modulators, both positive and negative, of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is inhibited. Opioids such as oxycodone also inhibit the release of vasopressin, somatostatin, insulin, and glucagon. Opioids close N-type voltage-operated calcium channels (kappa-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (mu and delta receptor agonist). This results in hyperpolarization and reduced neuronal excitability.</mechanism_of_action>
      <constants/>
      <references/>
    </target>
    <target>
      <target_id>BE0000770</target_id>
      <mechanism_of_action>Oxycodone acts as a weak agonist at mu, kappa, and delta opioid receptors within the central nervous system (CNS). Oxycodone primarily affects mu-type opioid receptors, which are coupled with G-protein receptors and function as modulators, both positive and negative, of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is inhibited. Opioids such as oxycodone also inhibit the release of vasopressin, somatostatin, insulin, and glucagon. Opioids close N-type voltage-operated calcium channels (kappa-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (mu and delta receptor agonist). This results in hyperpolarization and reduced neuronal excitability.</mechanism_of_action>
      <constants/>
      <references/>
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    <target>
      <target_id>BE0000420</target_id>
      <mechanism_of_action>Oxycodone acts as a weak agonist at mu, kappa, and delta opioid receptors within the central nervous system (CNS). Oxycodone primarily affects mu-type opioid receptors, which are coupled with G-protein receptors and function as modulators, both positive and negative, of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is inhibited. Opioids such as oxycodone also inhibit the release of vasopressin, somatostatin, insulin, and glucagon. Opioids close N-type voltage-operated calcium channels (kappa-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (mu and delta receptor agonist). This results in hyperpolarization and reduced neuronal excitability.</mechanism_of_action>
      <constants/>
      <references/>
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    <target>
      <target_id>BE0004899</target_id>
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      <constants/>
      <references/>
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      <target_id>BE0002226</target_id>
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  </targets>
</compound>
