Cocaine

For other uses, see Cocaine (disambiguation).

Cocaine
Clinical data
Pronunciationkə(ʊ)ˈkeɪn
Trade namesNeurocaine,[1] Goprelto,[2] Numbrino,[3] others
Other namesCoke, blow, snow, yay, crack (in free base form)
AHFS/Drugs.comMicromedex Detailed Consumer Information
License data
Dependence
liability		Physical: Low Psychological: High[4]
Addiction
liability		High[5]
Routes of
administration		Topical, by mouth, insufflation, intravenous, inhalation
Drug class
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability
MetabolismLiver, CYP3A4
MetabolitesNorcocaine, benzoylecgonine, cocaethylene
Onset of actionSeconds to minutes[12]
Duration of action20 to 90 minutes[12]
ExcretionKidney
Identifiers
  • Methyl (1R,2R,3S,5S)-3-(benzoyloxy)-8-methyl-8-azabicyclo[3.2.1]octane-2-carboxylate
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
PDB ligand
CompTox Dashboard (EPA)
ECHA InfoCard100.000.030 Edit this at Wikidata
Chemical and physical data
FormulaC17H21NO4
Molar mass303.358 g·mol−1
3D model (JSmol)
Melting point98 °C (208 °F)
Boiling point187 °C (369 °F)
Solubility in water1.8g/L (22 °C)
  • CN1[C@H]2CC[C@@H]1[C@@H](C(OC)=O)[C@@H](OC(C3=CC=CC=C3)=O)C2
  • InChI=1S/C17H21NO4/c1-18-12-8-9-13(18)15(17(20)21-2)14(10-12)22-16(19)11-6-4-3-5-7-11/h3-7,12-15H,8-10H2,1-2H3/t12-,13+,14-,15+/m0/s1 checkY
  • Key:ZPUCINDJVBIVPJ-LJISPDSOSA-N checkY
Data page
Cocaine (data page)
 ☒NcheckY (what is this?)  (verify)

Cocaine (from French cocaïne, from Spanish coca, ultimately from Quechua kúka)[13] is a tropane alkaloid that acts as a central nervous system (CNS) stimulant. As an extract, it is mainly used recreationally and often illegally for its euphoric and rewarding effects. It is also used in medicine by Indigenous South Americans for various purposes and rarely, but more formally, as a local anaesthetic or diagnostic tool by medical practitioners in more developed countries. It is primarily obtained from the leaves of two Coca species native to South America: Erythroxylum coca and E. novogranatense.[14][15] After extraction from the plant, and further processing into cocaine hydrochloride (powdered cocaine), the drug is administered by being either snorted, applied topically to the mouth, or dissolved and injected into a vein. It can also then be turned into free base form (typically crack cocaine), in which it can be heated until sublimated and then the vapours can be inhaled.[12]

Cocaine stimulates the mesolimbic pathway in the brain.[15] Mental effects may include an intense feeling of happiness, sexual arousal, loss of contact with reality, or agitation.[12] Physical effects may include a fast heart rate, sweating, and dilated pupils.[12] High doses can result in high blood pressure or high body temperature.[16] Onset of effects can begin within seconds to minutes of use, depending on method of delivery, and can last between five and ninety minutes.[12] As cocaine also has numbing and blood vessel constriction properties, it is occasionally used during surgery on the throat or inside of the nose to control pain, bleeding, and vocal cord spasm.[17]

Cocaine crosses the blood–brain barrier via a proton-coupled organic cation antiporter[18][19] and (to a lesser extent) via passive diffusion across cell membranes.[20] Cocaine blocks the dopamine transporter,[21] inhibiting reuptake of dopamine from the synaptic cleft into the pre-synaptic axon terminal; the higher dopamine levels in the synaptic cleft increase dopamine receptor activation in the post-synaptic neuron,[22][23] causing euphoria and arousal.[24] Cocaine also blocks the serotonin transporter and norepinephrine transporter, inhibiting reuptake of serotonin and norepinephrine from the synaptic cleft into the pre-synaptic axon terminal and increasing activation of serotonin receptors and norepinephrine receptors in the post-synaptic neuron, contributing to the mental and physical effects of cocaine exposure.[6]

A single dose of cocaine induces tolerance to the drug's effects.[25] Repeated use is likely to result in addiction. Addicts who abstain from cocaine may experience prolonged craving lasting for many months.[26][27] Abstaining addicts also experience modest drug withdrawal symptoms lasting up to 24 hours, with sleep disruption, anxiety, irritability, crashing, depression, decreased libido, decreased ability to feel pleasure, and fatigue being common.[28][15] Use of cocaine increases the overall risk of death, and intravenous use potentially increases the risk of trauma and infectious diseases such as blood infections and HIV through the use of shared paraphernalia. It also increases risk of stroke, heart attack, cardiac arrhythmia, lung injury (when smoked), and sudden cardiac death.[15][29] Illicitly sold cocaine can be adulterated with fentanyl, local anesthetics, levamisole, cornstarch, quinine, or sugar, which can result in additional toxicity.[30][31] In 2017, the Global Burden of Disease study found that cocaine use caused around 7,300 deaths annually.[32]

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  2. ^ Cite error: The named reference Goprelto FDA label was invoked but never defined (see the help page).
  3. ^ Cite error: The named reference Numbrino FDA label was invoked but never defined (see the help page).
  4. ^ Ghodse H (2010). Ghodse's Drugs and Addictive Behaviour: A Guide to Treatment (4 ed.). Cambridge University Press. p. 91. ISBN 978-1-139-48567-8. Archived from the original on 10 September 2017.
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  12. ^ a b c d e f Zimmerman JL (October 2012). "Cocaine intoxication". Critical Care Clinics. 28 (4): 517–26. doi:10.1016/j.ccc.2012.07.003. PMID 22998988.
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  17. ^ Hamdan AL, Sataloff RT, Hawkshaw MJ (2022). "Topical Anesthesia in Office-Based Laryngeal Surgery". Office-Based Laryngeal Surgery. USA: Springer. pp. 123–137. doi:10.1007/978-3-030-91936-8_6. ISBN 978-3-030-91935-1. Archived from the original on 18 July 2022. Retrieved 18 July 2022.
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  19. ^ Tega Y, Tabata H, Kurosawa T, Kitamura A, Itagaki F, Oshitari T, et al. (January 2021). "Structural Requirements for Uptake of Diphenhydramine Analogs into hCMEC/D3 Cells Via the Proton-Coupled Organic Cation Antiporter". Journal of Pharmaceutical Sciences. 110 (1): 397–403. doi:10.1016/j.xphs.2020.09.001. PMID 32898521.
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  21. ^ Cheng MH, Block E, Hu F, Cobanoglu MC, Sorkin A, Bahar I (2015). "Insights into the Modulation of Dopamine Transporter Function by Amphetamine, Orphenadrine, and Cocaine Binding". Frontiers in Neurology. 6: 134. doi:10.3389/fneur.2015.00134. PMC 4460958. PMID 26106364.
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