Cocaine
| Clinical data | |
|---|---|
| Pronunciation | kə(ʊ)ˈkeɪn |
| Trade names | Neurocaine,[1] Goprelto,[2] Numbrino,[3] others |
| Other names | Benzoylmethylecogine |
| AHFS/Drugs.com | Micromedex 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 |
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| Pharmacokinetic data | |
| Bioavailability |
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| Metabolism | Liver, CYP3A4 |
| Metabolites | Norcocaine, benzoylecgonine, cocaethylene (when consumed with alcohol) |
| Onset of action | Seconds to minutes[13] |
| Duration of action | 20 to 90 minutes[13] |
| Excretion | Kidney |
| Identifiers | |
IUPAC name
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| CompTox Dashboard (EPA) | |
| ECHA InfoCard | 100.000.030 |
| Chemical and physical data | |
| Formula | C17H21NO4 |
| Molar mass | 303.358 g·mol−1 |
| 3D model (JSmol) | |
| Melting point | 98 °C (208 °F) |
| Boiling point | 187 °C (369 °F) |
| Solubility in water | 1.8g/L (22 °C) |
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| Cocaine (data page) | |
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Cocaine is a central nervous system stimulant and tropane alkaloid derived primarily from the leaves of two coca species native to South America: Erythroxylum coca and E. novogranatense.[14][15][16][17][18] Coca leaves are processed into cocaine paste, a crude mix of coca alkaloids which cocaine base is isolated and converted to cocaine hydrochloride, commonly known as "cocaine".[18] Cocaine was once a standard topical medication as a local anesthetic with intrinsic vasoconstrictor activity, but its high abuse potential, adverse effects, and cost have limited its use and led to its replacement by other medicines.[19][20][21] "Cocaine and its combinations" are formally excluded from the WHO Model List of Essential Medicines.[22]
Street cocaine is commonly snorted, injected, or smoked as crack cocaine, with effects lasting up to 90 minutes depending on the route.[13][23] Cocaine acts pharmacologically as a serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI),[7][24][17] producing reinforcing effects such as euphoria, increased alertness, concentration, libido, and reduced fatigue and appetite.[25]
Cocaine has numerous adverse effects. Acute use can cause vasoconstriction, tachycardia, hypertension, hyperthermia, seizures, while overdose may lead to stroke, heart attack, or sudden cardiac death.[17][13][26] Cocaine also produces a spectrum of psychiatric symptoms including agitation, paranoia, anxiety, irritability, stimulant psychosis, hallucinations, delusions, violence, as well as suicidal and homicidal thinking.[27][17] Prenatal exposure poses risks to fetal development.[28][29][30][31] Chronic use may result in cocaine dependence, withdrawal symptoms, neurotoxicity, and nasal damage, including cocaine-induced midline destructive lesions.[32][33][34][35][36][37] No approved medication exists for cocaine dependence, so psychosocial treatment is primary.[38][39] Cocaine is frequently laced with levamisole to increase bulk.[40][41] This is linked to vasculitis (CLIV) and autoimmune conditions (CLAAS).[42][43]
Coca cultivation and its subsequent processes occur primarily Latin America, especially in the Andes of Bolivia, Peru, and Colombia, though cultivation is expanding into Central America, including Honduras, Guatemala, and Belize.[18][44][45][46][47] Violence linked to the cocaine trade continues to affect Latin America and the Caribbean and is expanding into Western Europe, Asia, and Africa as transnational organized crime groups compete globally.[48][49] Cocaine remains the world’s fastest-growing illicit drug market.[50][51] Coca chewing dates back at least 8,000 years in South America.[52] Large-scale cultivation occurred in Taiwan and Java prior to World War II.[53][54] Decades later, the cocaine boom marked a sharp rise in illegal cocaine production and trade, beginning in the late 1970s and peaking in the 1980s.[55] Cocaine is regulated under international drug control conventions, though national laws vary: several countries have decriminalized small quantities.[56][57][58][59]
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- ^ Introduction to Pharmacology (3 ed.). Abingdon: CRC Press. 2007. pp. 222–223. ISBN 978-1-4200-4742-4. Archived from the original on 10 September 2017.
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- ^ a b c d Pomara C, Cassano T, D'Errico S, Bello S, Romano AD, Riezzo I, et al. (2012). "Data available on the extent of cocaine use and dependence: biochemistry, pharmacologic effects and global burden of disease of cocaine abusers". Current Medicinal Chemistry. 19 (33): 5647–57. doi:10.2174/092986712803988811. PMID 22856655.
- ^ a b c "Coca Cultivation in the Andean Region" (PDF). UNODC. June 2006.
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- ^ "WHO Model List of Essential Medicines - 23rd list, 2023". www.who.int.
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- ^ 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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- ^ Sordo L, Indave BI, Barrio G, Degenhardt L, de la Fuente L, Bravo MJ (September 2014). "Cocaine use and risk of stroke: a systematic review". Drug and Alcohol Dependence (Systematic Review). 142: 1–13. doi:10.1016/j.drugalcdep.2014.06.041. PMID 25066468.
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