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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. 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". Cocaine was once a standard topical medication, but its high abuse potential, adverse effects, and cost have limited its use and led to its replacement by other medicines. "Cocaine and its combinations" are formally excluded from the WHO Model List of Essential Medicines.
Street cocaine is commonly snorted, injected, or smoked as crack cocaine, with effects lasting up to 90 minutes depending on the route. Cocaine acts pharmacologically as a serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI), producing reinforcing effects such as euphoria, increased alertness, concentration, aphrodisiac, and reduced fatigue and Anorectic.
Cocaine has numerous . Acute use can cause vasoconstriction, tachycardia, hypertension, hyperthermia, seizures, while overdose may lead to stroke, heart attack, or sudden cardiac death. 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. Prenatal exposure poses risks to fetal development. Chronic use may result in cocaine dependence, withdrawal symptoms, neurotoxicity, and nasal damage, including cocaine-induced midline destructive lesions. No approved medication exists for cocaine dependence, so psychosocial treatment is primary. Cocaine is frequently laced with levamisole to increase bulk. This is linked to vasculitis () and Autoimmunity conditions ().
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. 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. Cocaine remains the world’s fastest-growing illicit drug market. Coca chewing dates back at least 8,000 years in South America. Large-scale cultivation occurred in Taiwan and Java prior to World War II. 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. Cocaine is regulated under international drug control conventions, though national laws vary: several countries have decriminalized small quantities.
Globally, in 2019, cocaine was used by an estimated 20 million people (0.4% of adults aged 15 to 64 years). The highest prevalence of cocaine use was in Australia and New Zealand (2.1%), followed by North America (2.1%), Western Europe and Central Europe (1.4%), and South America and Central America (1.0%). Since 1961, the Single Convention on Narcotic Drugs has required countries to make recreational use of cocaine a crime. In the United States, cocaine is regulated as a Schedule II drug under the Controlled Substances Act, meaning that it has a high potential for abuse but has an accepted medical use. While rarely used medically today, its accepted uses include serving as a topical local anesthetic for the upper respiratory tract and as an antihemorrhagic agent to stop bleeding in the mouth, throat, and nasal cavities.
In 1986 an article in the Journal of the American Medical Association revealed that U.S. health food stores were selling dried coca leaves to be prepared as an infusion as "Health Inca Tea". While the packaging claimed it had been "decocainized", no such process had actually taken place. The article stated that drinking two cups of the tea per day gave a mild stimulation, increased heart rate, and emotional mood elevation, and the tea was essentially harmless.
Today, the US Drug Enforcement Administration (DEA) classifies cocaine as a Schedule II drug, recognizing its high potential for abuse but still permitting its limited use for medical purposes. However, current pharmacoepidemiological trends suggest that cocaine may soon reach the point where, in practical terms, it is no longer used medically in health care as a Schedule II substance. This report may prompt some states (such as North Dakota) and institutions to reconsider whether further efforts to identify alternative agents are needed. As physician boards—but not pharmacy boards—continue to assess knowledge of licit cocaine, attention may shift toward drugs with more contemporary medical use.
Cocaine is rarely prescribed in modern medicine due to its high potential for abuse and significant risk of adverse effects; its use is now almost exclusively limited to health facility for specific diagnostic procedures or surgeries.
Nasal solution cocaine hydrochloride ( Goprelto), an ester used for intranasal application, was approved for medical use in the United States in December 2017, and is indicated for the introduction of topical anesthesia of the mucous membranes for diagnostic procedures and surgeries on or through the nasal cavities of adults. Cocaine hydrochloride ( Numbrino) was approved for medical use in the United States in January 2020. Headache and epistaxis are the most frequently reported adverse reactions with Goprelto, while hypertension and tachycardia-including sinus tachycardia-are most common with Numbrino.
However, apraclonidine has largely replaced cocaine as the first-line pharmacologic agent for the diagnosis of Horner syndrome in routine clinical practice.
Cocaine is a central nervous system stimulant. Its effects can last from 15 minutes to an hour. The duration of cocaine's effects depends on the amount taken and the route of administration. Cocaine can be in the form of fine white powder and has a bitter taste. Crack cocaine is a smokeable form of cocaine made into small "rocks" by processing cocaine with sodium bicarbonate (baking soda) and water.
Cocaine use leads to increases in alertness, feelings of well-being and euphoria, increased energy and motor control activity, and increased feelings of competence and Human sexuality.
Expectations about cocaine's effects—both positive and negative—can influence how people feel after using it. Surprisingly, expecting negative effects may increase the drug's perceived positive impact, making quitting or avoiding cocaine more difficult for some individuals.
Analysis of the correlation between the use of 18 various psychoactive substances shows that cocaine use correlates with other "Club drug" (such as MDMA or amphetamines), as well as with heroin and use, and can be considered as a bridge between the use of different groups of drugs. (2025). 9783030104412, Springer, Cham. ISBN 9783030104412
In a study of cocaine users, the average time taken to reach peak subjective effects was 14.6 minutes. Any damage to the inside of the nose is due to cocaine constricting blood vessels—and therefore restricting blood and oxygen/nutrient flow—to that area, which, after chronic use, may cause "cocaine nose."
Most banknotes have traces of cocaine on them; this has been confirmed by studies done in several countries. In 1994, the U.S. 9th Circuit Court of Appeals cited findings that in Los Angeles, three out of four banknotes were tainted by cocaine or another illicit drug.
, hollowed-out , cut drinking straw, pointed ends of keys, long fingernails or artificial nails, and (clean) tampon applicators are also used to insufflate cocaine. The cocaine typically is poured onto a flat, hard surface (such as a mobile phone screen, plate, mirror, CD case or book) and divided into "bumps", "lines" or "rails", and then insufflated. A 2001 study reported that the sharing of straws used to "snort" cocaine can spread blood diseases such as hepatitis C.
Crude cocaine preparation intermediates are marketed as cheaper alternatives to pure cocaine to local markets while the more expensive end product is exported to United States and European markets. Freebase cocaine paste preparations can be smoked. The psychological and physiological effects of the paco are quite severe. Media usually report that it is extremely toxic and addictive. According to a study by Intercambios, media appear to exaggerate the effects of paco. These stereotypes create a sense that nothing can be done to help a paco addict and thus stand in the way of rehabilitation programs.
Under the former FDA pregnancy category system, cocaine was classified as a Category C drug. Its potential to cause harm to the fetus is not fully known, so it should only be administered to pregnant women if clearly necessary.
Cocaine can act as a teratogen, having various effects on the developing fetus. Some common teratogenic defects caused by cocaine include hydronephrosis, cleft palate, polydactyly, and down syndrome. Cocaine as a drug has a low molecular weight and high water and lipid solubility which enables it to cross the placenta and fetal blood-brain barrier. Because cocaine is able to pass through the placenta and enter the fetus, the fetus' circulation can be negatively affected. With restriction of fetal circulation, the development of organs in the fetus can be impacted, even resulting in Gastroschisis of the fetus' body. Cocaine use during pregnancy can also result in obstetric labor complications such as, placental abruption, preterm birth or delivery, uterine rupture, miscarriage, and stillbirth. Prenatal cocaine exposure may cause subtle cognitive deficits and lower the chance of above-average IQ by age 4, but supportive caregiving can significantly improve outcomes.
The March of Dimes said "it is likely that cocaine will reach the baby through breast milk," and advises the following regarding cocaine use during pregnancy:
In the body, levamisole is converted into aminorex, a substance with amphetamine-like stimulant effects and a long duration of action. Levamisole-adulterated cocaine is associated with cocaine- and levamisole-induced vasculitis (CLIV) and cocaine/levamisole-associated autoimmune syndrome (CLAAS). Reagent testing kits can be used to detect the presence of cocaine and levamisole.
During the mid-2010s, levamisole was found in most cocaine products available in both the United States and Europe. Levamisole is known to cause an acute condition involving a severe and dangerous lowered white blood cell count, known as agranulocytosis, in cocaine users, and may also accentuate cocaine's effects.
Clinical studies have shown that taking levamisole at doses of 50–200 mg per day can lead to agranulocytosis in approximately 0.08–5% of patients.
Cocaine and levamisole-adulterated cocaine (LAC) can cause cocaine-induced vasculitis (CIV) that mimics primary anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), presenting as cocaine-induced midline destructive lesions, LAC vasculopathy, or CIV. These conditions involve immune activation through NETosis and ANCA formation, leading to injury. Diagnosis is challenging due to symptom overlap and undisclosed drug use, making clinical suspicion and drug history essential for proper management.
Levamisole has become a common additive to illicit cocaine. It is thought to intensify the "high" by releasing dopamine in the brain, acts as a bulking agent, and is a difficult adulterant to recognize. Potential risks of levamisole-laced cocaine include autoimmune disease, neutropenia, arthralgias, retiform purpura, skin necrosis, and fever.
Cocaine use damages gray matter in brain regions critical for memory, attention, and emotion, leading to cognitive and behavioral impairments. It also disrupts dopamine levels and blood flow, accelerating aging brain and causing long-term neurological harm.
A considerable proportion of cocaine addicts exhibit hypomanic personality traits that are ego-syntonic with their pattern of cocaine abuse.
Cocaine intoxication mirrors core traits of narcissism—both involve a dopamine-driven, compulsive drive for reward. Just as cocaine produces a brief high that temporarily enhances the sense of worth, narcissists rely on external admiration to feed an addiction to their self-esteem, resulting in a self-reinforcing feedback cycle.
The misuse of cocaine has a high correlation with suicide. In those who use cocaine, the risk is greatest during the withdrawal phase. Cocaine use has been linked to homicide, with up to 31% of homicide victims testing positive for the drug. In 1989 Fulton County, 40% of homicide victims had cocaine metabolites, especially Black and firearm victims.
A 2020 study found that men with cocaine use disorder have greater difficulty identifying emotional expression in female faces, affecting relationships and suggesting a target for intervention. A 2021 study found that cocaine use disorder impairs emotion recognition, especially for happiness and fear, with improvement after long-term abstinence.
Depression is modestly linked to current drug use in cocaine users but does not clearly predict treatment participation or future use. For people who use cocaine, stress and craving can make each other worse. This may help explain why stress can lead to relapse in people trying to stop using cocaine.
Cocaine-induced psychosis shows sensitization toward the psychotic effects of the drug. This means that psychosis becomes more severe with repeated intermittent use.
Acute exposure to cocaine has many effects on humans, including euphoria, increases in heart rate and blood pressure, and increases in cortisol secretion from the adrenal gland. In humans with acute exposure followed by continuous exposure to cocaine at a constant blood concentration, the acute tolerance to the chronotropic cardiac effects of cocaine begins after about 10 minutes, while acute tolerance to the euphoric effects of cocaine begins after about one hour. With excessive or prolonged use, the drug can cause , tachycardia, and formication. Cocaine can induce psychosis characterized by paranoia, impaired reality testing, hallucinations, irritability, and physical aggression. Cocaine intoxication can cause hyperawareness, hypervigilance, psychomotor agitation, and delirium. Consumption of large doses of cocaine can cause violent outbursts, especially by those with preexisting psychosis. Acute exposure may induce arrhythmia, including atrial fibrillation, supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation. Acute exposure may also lead to angina, heart attack, and congestive heart failure. Cocaine overdose may cause seizures, hyperthermia and a marked elevation of blood pressure, which can be life-threatening, Heart arrhythmia, and death. Anxiety, paranoia, and restlessness can also occur, especially during the comedown. With excessive dosage, , , and Hypothermia are observed.
Cocaine use leads to an increased risk of hemorrhagic and ischemic . Cocaine use also increases the risk of having a heart attack.
Cocaine use also promotes the thrombosis. This increase in blood clot formation is attributed to cocaine-associated increases in the activity of plasminogen activator inhibitor, and an increase in the number, activation, and aggregation of .
Cocaine Vasoconstriction, Mydriasis, and increases body temperature, heart rate, and blood pressure. It can also cause headaches and gastrointestinal complications such as abdominal pain and nausea. Chronic users may lose their appetite and experience severe malnutrition, leading to being underweight.
A 2014 study found that increased cocaine use is linked to greater cognitive impairment, particularly in working memory, while reduced or ceased use can lead to partial or full recovery of cognitive function. These findings suggest that some cocaine-related cognitive deficits are reversible, especially if use begins later in life. A 2018 review found little evidence that chronic cocaine use causes widespread cognitive impairment. Exposure to cocaine may lead to the breakdown of the blood–brain barrier. (2025). 9780123745040 ISBN 9780123745040
Cocaine use is frequently associated with involuntary tooth grinding, known as bruxism, which can cause dental attrition and gingivitis. Additionally, stimulants like cocaine, methamphetamine, and even caffeine cause dehydration and Xerostomia.
Withdrawal symptoms include disrupted sleep, irritability, depression, and reduced ability to experience pleasure (anhedonia). Chronic nasal use may cause destructive damage to the nasal septum, including cocaine-induced midline destructive lesions (CIMDL). Illicit cocaine is frequently adulterated with substances such as fentanyl, levamisole, or local anesthetics, increasing its toxicity. Concurrent use with alcohol produces cocaethylene, a metabolite that significantly increases the risk of sudden death. According to the Global Burden of Disease Study, cocaine use is responsible for approximately 7,300 deaths annually.
Cocaine abuse can trigger addiction-related structural neuroplasticity in the human brain, although the permanence of such changes remains uncertain. Genealogy is a known risk factor, as relatives of cocaine users have an increased likelihood of developing cocaine addiction.
A key mechanism involves the overexpression of ΔFosB in the nucleus accumbens, altering transcriptional regulation and reinforcing drug-seeking behavior. Each dose of cocaine raises ΔFosB levels without a known saturation point. This elevation leads to increased brain-derived neurotrophic factor (BDNF) levels, which in turn enhance dendrite branching and dendritic spine density in neurons of the nucleus accumbens and prefrontal cortex, potentially persisting for weeks after drug cessation. In transgenic mice engineered to express ΔFosB in the nucleus accumbens and dorsal striatum, heightened behavioral sensitization to cocaine has been observed. These mice self-administer cocaine at lower doses and display a greater propensity for relapse after withdrawal ΔFosB also enhances sensitivity to reward by upregulating the AMPA receptor subunit GluR2 and downregulating the expression of dynorphin.
Cocaine use has also been shown to increase DNA damage in the brains of rodents. During subsequent DNA repair, enduring alterations in chromatin structure may arise, such as DNA methylation and methylation or acetylation of histones at the repair loci. These modifications may result in lasting epigenetics, which are believed to contribute to the persistent epigenetic changes observed in cocaine addiction.
About 25% of adults with attention deficit hyperactivity disorder (ADHD) use cocaine, and 10% develop a cocaine use disorder during their lifetime. Because cocaine use can worsen health outcomes, adults with ADHD should be screened for cocaine use disorder and referred for treatment if needed.
Cocaine-dependent patients with high neuroticism scores are more likely to experience cocaine-induced psychotic symptoms, regardless of other drug use factors, making Personality test important for risk identification and patient warning.
Cocaine drug withdrawal symptoms group into two types: depressive (e.g., depression, craving, insomnia) and somatic (e.g., increased appetite, fatigue). Depressive symptoms are linked to worse outcomes like longer depression, treatment, and risky behaviors.
Cocaine Anonymous (CA) is a twelve-step program formed in 18 November 1982 for people who seek recovery from drug addiction. It is patterned very closely after Alcoholics Anonymous (AA), although the two groups are unaffiliated. While many CA members have been addicted to cocaine, crack, speed or similar substances, CA accepts all who desire freedom from "cocaine and all other mind-altering substances" as members.
Numerous medications have been investigated for use in cocaine dependence, but , none of them were considered to be effective. Drugs which help to re-stabilize the glutamate system such as N-acetylcysteine have been proposed for the treatment of addiction to cocaine, nicotine, and alcohol. However, none have sufficient evidence or regulatory approval for routine clinical use, so psychosocial interventions remain the mainstay of treatment.
About 30% of people who had snorted cocaine at least 25 times but less than daily, and 47% of daily users, reported experiencing nasal irritation, crusting or scabbing, and frequent nosebleeds. Cocaine use should be considered as a potential cause of persistent or unexplained rhinitis, including in adolescent patients.
Because the nose is a prominent facial feature, such visible damage often leads to embarrassment, stigma, and negative reactions from others. As a result, individuals with cocaine-induced nasal damage frequently withdraw from social activities and relationships, leading to social isolation. In many cases, this isolation is not just likely but almost inevitable, as affected individuals may feel unable to face the outside world due to the noticeable and sometimes severe changes to their appearance.
Nose disorders associated with cocaine nose include:
Chronic intranasal usage can degrade the cartilage separating the nostrils (the septum nasi), leading eventually to its complete disappearance.
Repair may involve rhinoplasty, which includes creating a new internal lining with nasolabial flaps and restoring support with costal cartilage grafts.
In 2024, Belgian doctors report a rise in patients needing nose reconstruction due to cocaine use, which damages nasal tissue and cartilage; however, few undergo surgery because it requires at least six months of abstinence from cocaine for proper healing.
Some individuals seek plastic surgery to repair or reconstruct nasal damage caused by cocaine use, although surgical outcomes can be complicated by ongoing tissue loss and poor healing. When nasal damage is too severe for reconstruction, a nose prosthesis may be used to restore appearance and quality of life.
Cocaine can be snorted, swallowed, injected, or smoked. Most deaths due to cocaine are accidental but may also be the result of body packing or stuffing with rupture in the gastrointestinal tract. Alcohol impairment increases the likelihood of risk-taking behaviors and susceptibility to peer pressure, and also raises the risk of overdose due to the formation of cocaethylene (see the alcohol section).
Use of cocaine causes abnormally fast heart rhythms and a marked elevation of blood pressure (hypertension), which can be life-threatening. This can lead to death from acute myocardial infarction, acute respiratory failure (i.e., hypoxemia, with or without hypercapnia), stroke, cerebral hemorrhage, and Cardiac arrest. Overdose can also cause acute hepatotoxicity—typically due to toxic metabolites—though most cases resolve quickly; however, fatal outcomes from multiple organ dysfunction syndrome are possible, and there is no specific antidote. Cocaine overdose may result in hyperthermia as stimulation and increased muscular activity cause greater heat production. Heat loss is also inhibited by the cocaine-induced vasoconstriction.
In 2024, drug-related deaths in England and Wales reached their highest level in three decades, with a notable increase in fatalities involving cocaine and experts urging urgent government intervention to address the crisis. Martin Powell, from the charity Transform, which campaigns for the legal regulation of drugs, suggested that the recent rise in cocaine-related deaths in the UK may be due to the increased purity of cocaine, leading users to consume it more frequently and alongside other substances.
Cocaine crosses the blood–brain barrier via both a proton-coupled organic cation antiporter and (to a lesser extent) via passive diffusion across cell membranes. As of September 2022, the gene or genes encoding the human proton-organic cation antiporter had not been identified.
Cocaine has a short elimination half-life of 0.7–1.5 hours and is extensively metabolism by Blood plasma esterases and also by liver , with only about 1% excreted unchanged in the urine. The metabolism is dominated by hydrolysis ester cleavage, so the eliminated metabolites consist mostly of benzoylecgonine (BE), the major metabolite, and other metabolites in lesser amounts such as ecgonine methyl ester (EME) and ecgonine. Further minor metabolites of cocaine include norcocaine, p-hydroxycocaine, m-hydroxycocaine, p-hydroxybenzoylecgonine (), and m-hydroxybenzoylecgonine.
Depending on liver and kidney functions, cocaine metabolites are detectable in urine between three and eight days. Generally speaking benzoylecgonine is eliminated from someone's urine between three and five days. In urine from heavy cocaine users, benzoylecgonine can be detected within four hours after intake and in concentrations greater than 150 ng/mL for up to eight days later.
The pharmacodynamics of cocaine involve the complex relationships of neurotransmitters (inhibiting monoamine uptake in rats with ratios of about: serotonin:dopamine = 2:3, serotonin:norepinephrine = 2:5). (Table V. on page 37) The most extensively studied effect of cocaine on the central nervous system is the blockade of the dopamine transporter protein. Dopamine neurotransmitter released during neural signaling is normally recycled via the transporter; i.e., the transporter binds the transmitter and pumps it out of the synaptic cleft back into the presynaptic neuron, where it is taken up into storage vesicles. Cocaine binds tightly at the dopamine transporter forming a complex that blocks the transporter's function. The dopamine transporter can no longer perform its reuptake function, and thus dopamine accumulates in the synaptic cleft. The increased concentration of dopamine in the synapse activates post-synaptic dopamine receptors, which makes the drug Reward system and promotes the compulsive use of cocaine.
Cocaine affects certain serotonin (5-HT) receptors; in particular, it has been shown to antagonize the 5-HT3 receptor, which is a ligand-gated ion channel. An overabundance of 5-HT3 receptors is reported in cocaine-conditioned rats, though 5-HT3's role is unclear. The 5-HT2 receptor (particularly the subtypes 5-HT2A, 5-HT2B and 5-HT2C) are involved in the locomotor-activating effects of cocaine.
Cocaine has been demonstrated to bind as to directly stabilize the DAT transporter on the open outward-facing conformation. Further, cocaine binds in such a way as to inhibit a hydrogen bond innate to DAT. Cocaine's binding properties are such that it attaches so this hydrogen bond will not form and is blocked from formation due to the tightly locked orientation of the cocaine molecule. Research studies have suggested that the affinity for the transporter is not what is involved in the habituation of the substance so much as the conformation and binding properties to where and how on the transporter the molecule binds.
Conflicting findings have challenged the widely accepted view that cocaine functions solely as a reuptake inhibitor. To induce euphoria an intravenous dose of 0.3-0.6 mg/kg of cocaine is required, which blocks 66-70% of DAT in the brain. Re-administering cocaine beyond this threshold does not significantly increase DAT occupancy but still results in an increase of euphoria which cannot be explained by reuptake inhibition alone. This discrepancy is not shared with other dopamine reuptake inhibitors like bupropion, sibutramine, mazindol or tesofensine, which have similar or higher potencies than cocaine as dopamine reuptake inhibitors. Furthermore, a similar response-occupancy discrepancy has been observed with methylphenidate, which also stabilizes the dopamine transporter in an open outward-facing conformation. These findings have evoked a hypothesis that cocaine may also function as a so-called "DAT inverse agonist" or "negative allosteric modifier of DAT" resulting in dopamine transporter reversal, and subsequent dopamine release into the synaptic cleft from the axon terminal in a manner similar to but distinct from .
are affected by cocaine, as cocaine functions as a sigma ligand agonist. Further specific receptors it has been demonstrated to function on are NMDA and the D1 dopamine receptor.
Cocaine also blocks ion channel, thereby interfering with the propagation of ; thus, like lignocaine and novocaine, it acts as a local anesthetic. It also functions on the binding sites to the dopamine and serotonin sodium dependent transport area as targets as separate mechanisms from its reuptake of those transporters; unique to its local anesthetic value which makes it in a class of functionality different from both its own derived analogues which have that removed. In addition to this, cocaine has some target binding to the site of the κ-opioid receptor. Cocaine also causes vasoconstriction, thus reducing bleeding during minor surgical procedures. Recent research points to an important role of circadian mechanisms and clock genes in behavioral actions of cocaine.
Cocaine is known to suppress hunger and appetite by increasing co-localization of sigma σ1R receptors and ghrelin GHS-R1a cell surface receptors, thereby increasing ghrelin-mediated signaling of satiety and possibly via other effects on appetitive hormones.
Cocaine effects, further, are shown to be potentiated for the user when used in conjunction with new surroundings and stimuli, and otherwise novel environs.
Cocaine contains four chiral centers (1 R, 2 R, 3 S, and 5 S), two of which are configurationally dependent, resulting in eight possible . The formation of inactive stereoisomers, along with various synthetic by-products, limits both the yield and purity of the final product.
Although the chemical synthesis of cocaine is technically feasible, it is generally considered impractical due to its high cost, low efficiency, and challenges in stereoselective synthesis compared to extraction from natural plant sources. While domestic clandestine laboratories could theoretically reduce reliance on offshore production and international smuggling—as seen with illicit methamphetamine—manufacture and synthetic production of cocaine remains rare. Large-scale commercial synthesis has not been explored.
Large-scale biosynthesis of cocaine is unexplored.
The biosynthesis of cocaine has long attracted the attention of biochemists and organic chemists. This interest is partly motivated by the strong physiological effects of cocaine, but a further incentive was the unusual bicyclic structure of the molecule. The biosynthesis can be viewed as occurring in two phases, one phase leading to the N-methylpyrrolinium ring, which is preserved in the final product. The second phase incorporates a C4 unit with formation of the bicyclic tropane core.
However, since N. benthamiana also naturally contains nicotine, separating the cocaine from nicotine and related alkaloids would be challenging.
A Newsbeat investigation found that "cocaine torches" used by UK police to detect cocaine use are ineffective on typical street cocaine, as independent lab tests showed they fail to make the drug fluoresce. Experts and drug charities criticized the devices, warning they can give false positives and waste resources, while police forces defended their use as a deterrent. The manufacturer says the torches only work on much purer forms of cocaine than are found on the street.
Cocaine may be detected by law enforcement using the Scott reagent. The test can easily generate false positives for common substances and must be confirmed with a laboratory test.
Approximate cocaine purity can be determined using 1 mL 2% cupric sulfate pentahydrate in dilute HCl, 1 mL 2% potassium thiocyanate and 2 mL of chloroform. The shade of brown shown by the chloroform is proportional to the cocaine content. This test is not cross sensitive to heroin, methamphetamine, benzocaine, procaine and a number of other drugs but other chemicals could cause false positives.
Cocaine is prohibited in competition for athletes by the World Anti-Doping Agency (WADA), which lists it as a stimulant on its International Standard for the Prohibited List.
Fishscale cocaine, from fish + scale, is named for its shiny, yellowish flakes that resemble fish scales—distinct from the dull white appearance of standard cocaine powder.
Some countries, such as Bolivia, Colombia, and Peru, permit the cultivation of coca leaf for traditional consumption by the local indigenous population, but nevertheless, prohibit the production, sale, and consumption of cocaine. The provisions as to how much a coca farmer can yield annually is protected by laws such as the Bolivian Cato accord. In addition, some parts of Europe, the United States, and Australia allow processed cocaine for medicinal uses only.
In Western Australia under the Misuse of Drugs Act 1981 4.0g of cocaine is the amount of prohibited drugs determining a court of trial, 2.0g is the amount of cocaine required for the presumption of intention to sell or supply and 28.0g is the amount of cocaine required for purposes of drug trafficking.
Before the early 1900s, newspapers primarily portrayed addiction (rather than violence or crime) as the main problem caused by cocaine use, and depicted cocaine users as upper or middle class White people. In 1914, The New York Times published an article titled "Negro Cocaine 'Fiends' Are a New Southern Menace," portraying Black people who used cocaine as dangerous and able to withstand wounds that would normally be fatal. The Anti-Drug Abuse Act of 1986 mandated the same prison sentences for distributing 500 grams of powdered cocaine and just 5 grams of crack cocaine. In the National Survey on Drug Use and Health, white respondents reported a higher rate of powdered cocaine use, and Black respondents reported a higher rate of crack cocaine use.
The report further states that Western Europe’s cocaine market is rapidly expanding, resulting in increased violence driven by traffickers, including organized criminal groups from the Western Balkans. Concurrently, record levels of cocaine production have enabled traffickers to enter new markets across Asia and Africa, reflecting the expanding global reach of cocaine trafficking.
The U.S. is the world's largest consumer of cocaine, while South America, as a continent, ranks third in terms of consumer market size. Europe ranks cocaine as the second most commonly used illicit drug.
Cocaine is among the most widely consumed recreational stimulants worldwide.
One of the major implications of cocaine production is deforestation as large areas of forest are cleared for coca cultivation. The UNODC approximated that 97,622 hectares of primary forest were cleared for coca cultivation during 2001-2004 in the Andean region. This further causes habitat destruction, especially in biodiversity hotspots, areas rich in a variety of species. Such areas are chosen for coca cultivation due to their remote locations, minimising chances of detection. Deforestation has further = impacts of soil erosion which further inhibits the survival of native species.
The use of can also severely affect the environment. Farmers are able to use un-regulated and highly toxic pesticides due to the clandestine nature of drug production. The use of such pesticides can have both direct and indirect effects on the ecosystem. Where lethal levels of exposure directly cause the death of fauna, which is further carried up the food chain where secondary feeders who consume the poisoned animals are also impacted. Furthermore, non-lethal levels of exposure can also cause weaker immune system development and neurological issues, further increasing mortality rates.
The cocaine esterase enzyme and redesigned versions of it have been studied as a potential treatment for cocaine addiction in humans.
Coca tea has been explored as a supportive treatment for cocaine dependence. A study in Lima, Peru, found that using coca leaf infusion along with counseling reduced relapse rates and significantly increased the duration of abstinence among addicted individuals, suggesting that this approach may help prevent relapse during treatment.
Recent research has also examined the use of prescription psychostimulants for cocaine dependence, following the Self-Medication Hypothesis. This hypothesis suggests that some individuals use cocaine to address underlying neurochemical or psychological issues. While some studies indicate that psychostimulant therapy may reduce cocaine use and cravings, the evidence is mixed and further research is needed.
In animal studies, nicotine exposure in Laboratory mouse increases the likelihood of later cocaine use, with clear molecular changes in the brain. These findings mirror human Epidemiology data showing a link between nicotine use and increased risk of later cannabis and cocaine use, as well as other substances. Similarly, in rats, alcohol consumption raises the probability of later cocaine addiction and is associated with changes in the brain’s reward system. Human studies also show that alcohol use increases the risk of transitioning from cocaine use to addiction. (2025). 9780444635457 ISBN 9780444635457
Experimentally, cocaine injections can be delivered to animals such as fruit flies to study the mechanisms of cocaine addiction.
When the Spanish arrived in South America, they initially banned coca but soon legalized and taxed it after seeing its importance to local labor. The active ingredient, cocaine, was first isolated in 1855 by Friedrich Gaedcke and later refined by Albert Niemann, who named it “cocaine.” (2009). 9783764383367, Springer Science & Business Media. ISBN 9783764383367 In the late 1800s, cocaine became popular in Western medicine as a local anesthetic and was widely used in various products, including drinks and remedies. and James Leonard Corning demonstrated peridural anesthesia. However, due to its toxic effects and potential for abuse, safer alternatives eventually replaced it in medical practice.
Large-scale coca cultivation and cocaine production occurred in Taiwan Asia, in Taiwan (then known as Formosa) and Java (today part of Indonesia) before World War II.
Since the 1980s, the cocaine trade was dominated by centralized, hierarchical such as Medellín and Cali Cartel, along with their successors and early FARC factions. By the early 2000s, this model fragmented into a diverse network of global trafficking links, allowing South American cocaine production to easily supply markets in Europe, Africa, Asia, and Oceania through various routes.
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