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Stimulant
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Ritalin sustained-release (SR) 20 mg tablets
Cocaine is controlled drug, and it is a commonly used stimulant
Stimulants (also referred to as psychostimulants) is an overarching term that covers many drugs including those that increase activity of the body,[1] drugs that are pleasurable and invigorating, or drugs that have sympathomimetic effects.[2] Due to their rendering a characteristic "up" feeling, stimulants are also occasionally referred to as "uppers"[by whom?]. Stimulants are widely used throughout the world as prescription medicines as well as without a prescription (either legally or illicitly) as performance-enhancing or recreational drugs. The most frequently prescribed stimulants as of 2013 were lisdexamfetamine, methylphenidate, and amphetamine.[3] It is estimated that the percent of the population that has abused amphetamine-type stimulants (e.g., amphetamine, methamphetamine, MDMA, etc.) and cocaine combined is between .8% and 2.1%.[4]
Contents
[hide]
1 Effects
1.1 Acute
1.2 Chronic
2 Medical uses
3 Chemistry
3.1 Amphetamines (class)
3.2 Cocaine analogues
4 Mechanisms of action
5 Notable stimulants
5.1 Amphetamine
5.2 Caffeine
5.3 Ephedrine
5.4 MDMA
5.5 MDPV
5.6 Mephedrone
5.7 Methamphetamine
5.8 Methylphenidate
5.9 Nicotine
5.10 Phenylpropanolamine
5.11 Propylhexedrine
5.12 Pseudoephedrine
5.13 Catha edulis (Khat)
5.14 Cocaine
6 Abuse
7 Testing
8 See also
9 Notes
10 References
11 External links
Effects[edit]
Acute[edit]
Stimulants in therapeutic doses, such as those given to patients with ADHD, increases ability to focus, vigor, sociability, libido and may elevate mood. However, in higher doses stimulants may actually decrease the ability to focus, a principle of the Yerkes-Dodson Law. In higher doses stimulants may also produce euphoria, vigor, and decrease need for sleep. Many, but not all, stimulants have ergogenic effects. Drugs such as ephedrine, pseudoephedrine, amphetamine and methylphenidate have well documented ergogenic effects, while drugs such as cocaine and methamphetamine have the opposite effect.[5] Neurocognitive enhancing effects of stimulants, specifically modafinil, amphetamine and methylphenidate have been documented in healthy adolescents, and is a commonly cited reason among illicit drug users for use, particularly among college students in the context of studying.[6]
In some cases psychiatric phenomenon may emerge such as stimulant psychosis, paranoia, and suicidal ideation. Acute toxicity has been reportedly associated with a homicide, paranoia, aggressive behavior, motor dysfunction, and punding. The violent and aggressive behavior associated with acute stimulant toxicity may partially be driven by paranoia.[7] Most drugs classified as stimulants are sympathomimetics, that is they stimulate the sympathetic branch of the autonomic nervous system. This leads to effects such as mydriasis, increased heart rate, blood pressure, respiratory rate and body temperature.[8] When these changes become pathological, they are called arrhythmia, hypertension, and hyperthermia, and may lead to rhabdomyolysis, stroke, cardiac arrest, or seizures. However, given the complexity of the mechanisms that underly these potentially fatal outcomes of acute stimulant toxicity, it is impossible to determine what dose may be lethal.[9]
Chronic[edit]
Assessment of the effects of stimulants is relevant given the large population currently taking stimulants. A systematic review of cardiovascular effects of prescription stimulants found no association in children, but found a correlation between prescription stimulant use and ischemic heart attacks.[10] A review over a four-year period found that there were few negative effects of stimulant treatment, but stressed the need for longer term studies.[11] A review of a year long period of prescription stimulant use in those with ADHD found that cardiovascular side effects were limited to transient increases in blood pressure only.[12] Initiation of stimulant treatment in those with ADHD in early childhood appears to carry benefits into adulthood with regard to social and cognitive functioning, and appears to be relatively safe.[13]
Abuse of prescription stimulants (not following physician instruction) or of illicit stimulants carries many negative health risks. Abuse of cocaine, depending upon route of administration, increases risk of cardiorespiratory disease, stroke, and sepsis.[14] Some effects are dependent upon the route of administration, with intravenous use associated with the transmission of many disease such as Hepatitis C, HIV/AIDS and potential medical emergencies such as infection, thrombosis or pseudoaneurysm,[15] while inhalation may be associated with increased lower respiratory tract infection, lung cancer, and pathological restricting of lung tissue.[16] Cocaine may also increase risk for autoimmune disease[17][18][19] and damage nasal cartilage. Abuse of methamphetamine produces similar effects as well as marked degeneration of dopaminergic neurons, resulting in an increased risk for Parkinson's Disease.[20][21][22][23]
Medical uses[edit]
Stimulants have been used in medicine for many conditions including obesity, sleep disorders, mood disorders, impulse control disorders, asthma, nasal congestion and as anesthetics.[24] Drugs used to treat obesity are called anorectics and generally include drugs that follow the general definition of a stimulant, but other drugs such as CB1 receptor antagonists exist in this class too.[25][26] Drugs used to treat sleep disorders such as excessive daytime sleepiness are called eugeroics and include notable stimulants such as modafinil.[27][28] Stimulants are used in impulse control disorders such as ADHD[29] and off-label in mood disorders such as major depressive disorder to increase energy, focus and elevate mood.[30] Stimulants such as epinephrine,[31] theophylline and salbutamol[32] orally have been used to treat asthma, but inhaled adrenergic drugs are now preferred due to less systemic side effects. Pseudoephedrine is used to relieve nasal or sinus congestion caused by the common cold, sinusitis, hay fever and other respiratory allergies; it is also used to relieve ear congestion caused by ear inflammation or infection.[33][34]
Chemistry[edit]
For details on stimulant classes, see Substituted phenethylamine and Substituted amphetamine.
A chart comparing the chemical structures of different amphetamine derivatives
Classifying stimulants is difficult, because of the large number of classes the drugs occupy, and the fact that they may belong to multiple classes; for example, ecstasy can be classified as a substituted methylenedioxyphenethylamine, a substituted amphetamine and consequently, a substituted phenethylamine.[citation needed]
When referring to stimulants, the parent drug (e.g., amphetamine) will always be expressed in the singular[according to whom?]; with the word "substituted" placed before the parent drug (substituted amphetamines).
Major stimulant classes include phenethylamines and their daughter class substituted amphetamines.[according to whom?]
Amphetamines (class)[edit]
Main article: Substituted amphetamines
Substituted amphetamines are a class of compounds based upon the amphetamine structure;[35] it includes all derivative compounds which are formed by replacing, or substituting, one or more hydrogen atoms in the amphetamine core structure with substituents.[35][36][37] Examples of substituted amphetamines are amphetamine (itself),[35][36] methamphetamine,[35] ephedrine,[35] cathinone,[35] phentermine,[35] mephentermine,[35] bupropion,[35] methoxyphenamine,[35] selegiline,[35] amfepramone,[35] pyrovalerone,[35] MDMA (ecstasy), and DOM (STP). Many drugs in this class work primarily by activating trace amine-associated receptor 1 (TAAR1);[38] in turn, this causes reuptake inhibition and effluxion, or release, of dopamine, norepinephrine, and serotonin.[38] An additional mechanism of some substituted amphetamines is the release of vesicular stores of monoamine neurotransmitters through VMAT2, thereby increasing the concentration of these neurotransmitters in the cytosol, or intracellular fluid, of the presynaptic neuron.[39]
Amphetamines-type stimulants are often used for their therapeutic effects. Physicians sometimes prescribe amphetamine to treat major depression, where subjects do not respond well to traditional SSRI medications,[citation needed] but evidence supporting this use is poor/mixed.[40] Notably, two recent large phase III studies of lisdexamfetamine (a prodrug to amphetamine) as an adjunct to an SSRI or SNRI in the treatment of major depressive disorder showed no further benefit relative to placebo in effectiveness.[41] Numerous studies have demonstrated the effectiveness of drugs such as Adderall (a mixture of salts of amphetamine and dextroamphetamine) in controlling symptoms associated with ADHD. Due to their availability and fast-acting effects, substituted amphetamines are prime candidates for abuse.[42]
Cocaine analogues[edit]
Main article: List of cocaine analogues
Hundreds of cocaine analogues have been created, all of them usually maintaining a benzyloxy connected to the 3 carbon of a tropane. Various modifications include substitutions on the benzene ring, as well as additions or substitutions in place of the normal carboxylate on the tropane 2 carbon. Various compound with similar structure activity relationships to cocaine that aren't technically analogues have been developed as well.
Mechanisms of action[edit]
See also: central fatigue
Stimulants can have a wide variety of mechanisms. Many stimulants exert their effects through manipulations of monoamine neurotransmission. Monoamines are a class of neurotransmitter relevant in reward, motivation, temperature regulation and pain sensation that include dopamine, norepinephrine, and serotonin. Stimulants usually block the reuptake or stimulate the efflux of dopamine and norepinephrine resulting in increased activity of their circuits. Some stimulants, notably those with empathogenic and hallucinogenic effects alter serotonergic neurotransmission. Interference with vesicular storage, activating TAAR1, and reversing the flow of monoamine transporters may play a mechanism in the activity of these drugs. Adrenergic stimulants, such as ephedrine, may act by directly binding and activating the receptors that norepinephrine and epinephrine normally bind to(adrenergic receptors), producing sympathomimetic effects. Some drugs, such as MDMA and derivatives may decrease regulatory capability by antagonizing regulatory pre-synaptic auto receptors.[43] Caffeine is a notable exception, as it exerts its effects by antagonizing adenosine receptors instead of acting directly on monoamines.[44]
Notable stimulants[edit]
Amphetamine[edit]
Main article: Amphetamine
Amphetamine is a potent central nervous system (CNS) stimulant of the phenethylamine class that is approved for the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy.[45] Amphetamine was discovered in 1887 and exists as two enantiomers: levoamphetamine and dextroamphetamine.[note 1][46] Amphetamine refers to equal parts of the enantiomers, i.e., 50% levoamphetamine and 50% dextroamphetamine.[47][48] Amphetamine is also used as a performance and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant.[49][50][51][52] Although it is a prescription medication in many countries, unauthorized possession and distribution of amphetamine is often tightly controlled due to the significant health risks associated with uncontrolled or heavy use.[53][54] As a consequence, amphetamine is illegally synthesized by clandestine chemists, trafficked, and sold.[55] Based upon drug and drug precursor seizures worldwide, illicit amphetamine production and trafficking is much less prevalent than that of methamphetamine.[55]
The first pharmaceutical amphetamine was Benzedrine, a brand of inhalers used to treat a variety of conditions.[46][56] Because the dextro isomer has greater stimulant properties, Benzedrine was gradually discontinued in favor of formulations containing all or mostly dextroamphetamine. Presently, it is typically prescribed as Adderall, dextroamphetamine (e.g., Dexedrine), or the inactive prodrug lisdexamfetamine (e.g., Vyvanse).[46][57] Amphetamine, through activation of a trace amine receptor, increases biogenic amine and excitatory neurotransmitter activity in the brain, with its most pronounced effects targeting the catecholamine neurotransmitters norepinephrine and dopamine.[38] At therapeutic doses, this causes emotional and cognitive effects such as euphoria, change in libido, increased arousal, and improved cognitive control.[50][51][58] Likewise, it induces physical effects such as decreased reaction time, fatigue resistance, and increased muscle strength.[49]
In contrast, much larger doses of amphetamine are likely to impair cognitive function and induce rapid muscle breakdown.[45][50][59] Substance dependence (i.e., addiction) is a serious risk of amphetamine abuse, but only rarely arises from proper medical use.[45][60] Very high doses can result in a psychosis (e.g., delusions and paranoia), which very rarely occurs at therapeutic doses even during long-term use.[61][62] As recreational doses are generally much larger than prescribed therapeutic doses, recreational use carries a far greater risk of serious side effects.[45][59]
Caffeine[edit]
Main article: Caffeine
Roasted coffee beans, a common source of caffeine.
Caffeine is a stimulant compound belonging to the xanthine class of chemicals naturally found in coffee, tea, and (to a lesser degree) cocoa or chocolate. It is included in many soft drinks, as well as a larger amount in energy drinks. Caffeine is the world's most widely used psychoactive drug and by far the most common stimulant. In North America, 90% of adults consume caffeine daily.[63] A few jurisdictions restrict its sale and use. Caffeine is also included in some medications, usually for the purpose of enhancing the effect of the primary ingredient, or reducing one of its side-effects (especially drowsiness). Tablets containing standardized doses of caffeine are also widely available.
Caffeine's mechanism of action differs from many stimulants, as it produces stimulant effects by inhibiting adenosine receptors.[64] Adenosine receptors are thought to be a large driver of drowsiness and sleep, and their action increases with extended wakefulness.[65] Caffeine has been found to increase striatal dopamine in animal models,[66] as well as inhibit the inhibitory effect of adenosine receptors on dopamine receptors,[67] however the implications for humans are unknown. Unlike most stimulants, caffeine has no addictive potential. Caffeine does not appear to be a reinforcing stimulus, and some degree of aversion may actually occur, which people preferring placebo over caffeine in a study on drug abuse liability published in an NIDA research monograph.[68] In large telephone surveys only 11% reported dependence symptoms. However, when people were tested in labs, only half of those who claim dependence actually experienced it, casting doubt on caffeine's ability to produce dependence and putting societal pressures in the spotlight.[69]
Coffee consumption is associated with a lower overall risk of cancer.[70] This is primarily due to a decrease in the risks of hepatocellular and endometrial cancer, but it may also have a modest effect on colorectal cancer.[71] There does not appear to be a significant protective effect against other types of cancers, and heavy coffee consumption may increase the risk of bladder cancer.[71] A protective effect of caffeine against Alzheimer's disease is possible, but the evidence is inconclusive.[72][73][74] Moderate coffee consumption may decrease the risk of cardiovascular disease,[75] and it may somewhat reduce the risk of type 2 diabetes.[76] Drinking four or more cups of coffee per day does not affect the risk of hypertension compared to drinking little or no coffee. However those who drink 1–3 cups per day may be at a slightly increased risk.[77] Caffeine increases intraocular pressure in those with glaucoma but does not appear to affect normal individuals.[78] It may protect people from liver cirrhosis.[79] There is no evidence that coffee stunts a child's growth.[80] Caffeine may increase the effectiveness of some medications including ones used to treat headaches.[81] Caffeine may lessen the severity of acute mountain sickness if taken a few hours prior to attaining a high altitude.[82]
Ephedrine[edit]
Main article: Ephedrine
Ephedrine is a sympathomimetic amine similar in molecular structure to the well-known drugs phenylpropanolamine and methamphetamine, as well as to the important neurotransmitter epinephrine (adrenaline). Ephedrine is commonly used as a stimulant, appetite suppressant, concentration aid, and decongestant, and to treat hypotension associated with anaesthesia.
In chemical terms, it is an alkaloid with a phenethylamine skeleton found in various plants in the genus Ephedra (family Ephedraceae). It works mainly by increasing the activity of norepinephrine (noradrenaline) on adrenergic receptors.[83] It is most usually marketed as the hydrochloride or sulfate salt.
The herb má huáng (Ephedra sinica), used in traditional Chinese medicine (TCM), contains ephedrine and pseudoephedrine as its principal active constituents. The same may be true of other herbal products containing extracts from other Ephedra species.
MDMA[edit]
Tablets containing MDMA
Main article: MDMA
See also: Its parent class and MDA
3,4-Methylenedioxymethamphetamine (MDMA, ecstasy, or molly) is a euphoriant, empathogen, and stimulant of the amphetamine class.[84] Briefly used by some psychotherapists as an adjunct to therapy, the drug became popular recreationally and the DEA listed MDMA as a Schedule I controlled substance, prohibiting most medical studies and applications. MDMA is known for its entactogenic properties. The stimulant effects of MDMA include hypertension, anorexia (appetite loss), euphoria, social disinhibition, insomnia (enhanced wakefulness/inability to sleep), improved energy, increased arousal, and increased perspiration, among others. MDMA differs from most stimulants in that its primary pharmacological effect is on the neurotransmitter serotonin rather than dopamine, or norepinephrine. MDMA does not appear to be significantly addictive or dependence forming.[85]
Due to the relative safety of MDMA, some researchers such as David Nutt have criticized the scheduling level, writing a satirical article finding MDMA to be 28 times less dangerous than horseriding, a condition he termed "equasy" or "Equine Addiction Syndrome".[86]
MDPV[edit]
Main article: MDPV
Methylenedioxypyrovalerone (MDPV) is a psychoactive drug with stimulant properties that acts as a norepinephrine-dopamine reuptake inhibitor (NDRI).[87] It was first developed in the 1960s by a team at Boehringer Ingelheim.[88] MDPV remained an obscure stimulant until around 2004, when it was reported to be sold as a designer drug. Products labeled as bath salts containing MDPV were previously sold as recreational drugs in gas stations and convenience stores in the United States, similar to the marketing for Spice and K2 as incense.[89][90]
Incidents of psychological and physical harm have been attributed to MDPV use.[91][92]
Mephedrone[edit]
Main article: Mephedrone
Mephedrone is a synthetic stimulant drug of the amphetamine and cathinone classes. Slang names include drone[93] and MCAT.[94] It is reported to be manufactured in China and is chemically similar to the cathinone compounds found in the khat plant of eastern Africa. It comes in the form of tablets or a powder, which users can swallow, snort, or inject, producing similar effects to MDMA, amphetamines, and cocaine.
Mephedrone was first synthesized in 1929, but did not become widely known until it was rediscovered in 2003. By 2007, mephedrone was reported to be available for sale on the Internet; by 2008 law enforcement agencies had become aware of the compound; and, by 2010, it had been reported in most of Europe, becoming particularly prevalent in the United Kingdom. Mephedrone was first made illegal in Israel in 2008, followed by Sweden later that year. In 2010, it was made illegal in many European countries, and, in December 2010, the EU ruled it illegal. In Australia, New Zealand, and the USA, it is considered an analog of other illegal drugs and can be controlled by laws similar to the Federal Analog Act. In September 2011, the USA temporarily classified mephedrone as illegal, in effect from October 2011.
Methamphetamine[edit]
Main article: Methamphetamine
Methamphetamine (contracted from N-methyl-alpha-methylphenethylamine) is a neurotoxin and potent psychostimulant of the phenethylamine and amphetamine classes that is used to treat attention deficit hyperactivity disorder (ADHD) and obesity.[95][96][97] Methamphetamine exists as two enantiomers, dextrorotary and levorotary.[98][99] Dextromethamphetamine is a stronger CNS stimulant than levomethamphetamine;[59][98][99] however, both are addictive and produce the same toxicity symptoms at high doses.[99] Although rarely prescribed due to the potential risks, methamphetamine hydrochloride is approved by the United States Food and Drug Administration (USFDA) under the trade name Desoxyn.[96] Recreationally, methamphetamine is used to increase sexual desire, lift the mood, and increase energy, allowing some users to engage in sexual activity continuously for several days straight.[96][100]
Methamphetamine may be sold illicitly, either as pure dextromethamphetamine or in an equal parts mixture of the right- and left-handed molecules (i.e., 50% levomethamphetamine and 50% dextromethamphetamine).[100] Both dextromethamphetamine and racemic methamphetamine are schedule II controlled substances in the United States.[96] Also, the production, distribution, sale, and possession of methamphetamine is restricted or illegal in many other countries due to its placement in schedule II of the United Nations Convention on Psychotropic Substances treaty.[101][102] In contrast, levomethamphetamine is an over-the-counter drug in the United States.[note 2]
In low doses, methamphetamine can cause an elevated mood and increase alertness, concentration, and energy in fatigued individuals.[59][96] At higher doses, it can induce psychosis, rhabdomyolysis, and cerebral hemorrhage.[59][96] Methamphetamine is known to have a high potential for abuse and addiction.[59][96] Recreational use of methamphetamine may result in psychosis or lead to post-withdrawal syndrome, a withdrawal syndrome that can persist for months beyond the typical withdrawal period.[105] Unlike amphetamine and cocaine, methamphetamine is neurotoxic to humans, damaging both dopamine and serotonin neurons in the central nervous system (CNS).[95][97] Entirely opposite to the long-term use of amphetamine, there is evidence that methamphetamine causes brain damage from long-term use in humans;[95][97] this damage includes adverse changes in brain structure and function, such as reductions in gray matter volume in several brain regions and adverse changes in markers of metabolic integrity.[106][107][97]
Methylphenidate[edit]
Main article: Methylphenidate
Methylphenidate is a stimulant drug that is often used in the treatment of ADHD and narcolepsy and occasionally to treat obesity in combination with diet restraints and exercise. Its effects at therapeutic doses include increased focus, increased alertness, decreased appetite, decreased need for sleep and decreased impulsivity. Methylphenidate is not usually used recreationally, but when it is used, its effects are very similar to those of amphetamines.
Methylphenidate acts a norepinephrine-dopamine reuptake inhibitor, by blocking the norepinephrine transporter (NET) and the dopamine transporter (DAT). Methylphenidate has a higher affinity for the dopamine transporter than for the norepinephrine transporter, and so its effects are mainly due to elevated dopamine levels caused by the inhibited reuptake of dopamine, however increased norepinephrine levels also contribute to various of the effects caused by the drug.
Methylphenidate is sold in many forms, its most common trade name is the oral tablet Ritalin. Other versions include the long lasting tablet Concerta and the long lasting transdermal patch Daytrana.
Nicotine[edit]
Main article: Nicotine
Nicotine is the active chemical constituent in tobacco, which is available in many forms, including cigarettes, cigars, chewing tobacco, and smoking cessation aids such as nicotine patches, nicotine gum, and electronic cigarettes. Nicotine is used widely throughout the world for its stimulating and relaxing effects. Nicotine exerts its effects through the agonism of nicotinic acetylcholine receptor, resulting in multiple downstream effects such as increase in activity of dopaminergic neurons in the midbrain reward system, as well as the decreased expression of monoamine oxidase in the brain.[108] Nicotine is addictive and dependence forming. The most common source of nicotine, tobacco's, overall harm to user and self score as determined by a multi-criteria decision analysis was determined at 3 percent below cocaine, and 13 percent above amphetamines, ranking 6th most harmful of the 20 drugs assessed.[109]
Phenylpropanolamine[edit]
Main article: Phenylpropanolamine
Phenylpropanolamine (PPA; Accutrim; β-hydroxyamphetamine), also known as the stereoisomers norephedrine and norpseudoephedrine, is a psychoactive drug of the phenethylamine and amphetamine chemical classes that is used as a stimulant, decongestant, and anorectic agent.[110] It is commonly used in prescription and over-the-counter cough and cold preparations. In veterinary medicine, it is used to control urinary incontinence in dogs under trade names Propalin and Proin.
In the United States, PPA is no longer sold without a prescription due to a proposed increased risk of stroke in younger women. In a few countries in Europe, however, it is still available either by prescription or sometimes over-the-counter. In Canada, it was withdrawn from the market on 31 May 2001.[111] In India, human use of PPA and its formulations were banned on 10 February 2011.[112]
Propylhexedrine[edit]
Main article: Propylhexedrine
Propylhexedrine (Hexahydromethamphetamine, Obesin) is a stimulant medication, sold over-the-counter in the United States as the cold medication Benzedrex.[113] The drug has also been used as an appetite suppressant in Europe. Propylhexedrine is not an amphetamine, though it is structurally similar; it is instead a cycloalkylamine, and thus has stimulant effects that are less potent than similarly structured amphetamines, such as methamphetamine.
The abuse potential of propylhexedrine is fairly limited, due its limited routes of administration: in the United States, Benzedrex is only available as an inhalant, mixed with lavender oil and menthol. These ingredients cause unpleasant tastes, and abusers of the drug have reported unpleasant "menthol burps." Injection of the drug has been found to cause transient diplopia and brain stem dysfunction.[114][115][116]
Pseudoephedrine[edit]
Main article: Pseudoephedrine
Pseudoephedrine is a sympathomimetic drug of the phenethylamine and amphetamine chemical classes. It may be used as a nasal/sinus decongestant, as a stimulant,[117] or as a wakefulness-promoting agent.[118]
The salts pseudoephedrine hydrochloride and pseudoephedrine sulfate are found in many over-the-counter preparations, either as a single ingredient or (more commonly) in combination with antihistamines, guaifenesin, dextromethorphan, and/or paracetamol (acetaminophen) or another NSAID (such as aspirin or ibuprofen). It is also used as a precursor chemical in the illegal production of methamphetamine.
Catha edulis (Khat)[edit]
Main article: Khat
Catha edulis
Khat is a flowering plant native to the Horn of Africa and the Arabian Peninsula.[119][120]
Khat contains a monoamine alkaloid called cathinone, a "keto-amphetamine", that is said to cause excitement, loss of appetite, and euphoria. In 1980, the World Health Organization (WHO) classified it as a drug of abuse that can produce mild to moderate psychological dependence (less than tobacco or alcohol),[121] although the WHO does not consider khat to be seriously addictive.[120] It is a controlled substance in some countries, such as the United States, Canada, and Germany, while its production, sale, and consumption are legal in other nations, including Djibouti, Ethiopia, Somalia, and Yemen.[122]
Cocaine[edit]
Main article: Cocaine
Cocaine is an SNDRI. Cocaine is made from the leaves of the coca shrub, which grows in the mountain regions of South American countries such as Bolivia, Colombia, and Peru. In Europe, North America, and some parts of Asia, the most common form of cocaine is a white crystalline powder. Cocaine is a stimulant but is not normally prescribed therapeutically for its stimulant properties, although it sees clinical use as a local anesthetic, in particular in ophthalmology. Most cocaine use is recreational and its abuse potential is high (higher than amphetamine), and so its sale and possession are strictly controlled in most jurisdictions. Other tropane derivative drugs related to cocaine are also known such as troparil and lometopane but have not been widely sold or used recreationally.[123]
Abuse[edit]
Main article: Recreational drug use § Stimulants
See also: Substance abuse
Abuse of central nervous system (CNS) stimulants is common. Addiction to some CNS stimulants can quickly lead to medical, psychiatric, and psychosocial deterioration. Drug tolerance, dependence, and sensitization as well as a withdrawal syndrome can occur.[124]
Stimulants enhance the activity of the central and peripheral nervous systems. Common effects may include increased alertness, awareness, wakefulness, endurance, productivity, and motivation, arousal, locomotion, heart rate, and blood pressure, and a diminished desire for food and sleep.
Use of stimulants may cause the body to reduce significantly its production of natural body chemicals that fulfill similar functions. Until the body reestablishes its normal state, once the effect of the ingested stimulant has worn off the user may feel depressed, lethargic, confused, and miserable. This is referred to as a "crash", and may provoke reuse of the stimulant.
Stimulants may be screened for in animal discrimination and self-administration models which have high sensitivity albeit low specificity.[125] Research on a progressive ratio Self-administration protocol has found amphetamine, methylphenidate, modafinil, cocaine, and nicotine to all have a higher break point than placebo that scales with dose indicating reinforcing effects.[126]
Drug
Mean
Pleasure
Psychological dependence
Physical dependence.[127]
Cocaine 2.39 3.0 2.8 1.3
Tobacco 2.21 2.3 2.6 1.8
Amphetamine 1.67 2.0 1.9 1.1
Ecstasy 1.13 1.5 1.2 0.7
Testing[edit]
The presence of stimulants in the body may be tested by a variety of procedures. Serum and urine are the common sources of testing material although saliva is sometimes used. Commonly used tests include chromatography, immunologic assay, and mass spectrometry.[128]
See also[edit]
Antipsychotics
Depressants
Hallucinogens
Nootropics
Psychoanaleptics
Notes[edit]
Jump up ^ Enantiomers are molecules that are mirror images of one another; they are structurally identical, but of the opposite orientation.
Levoamphetamine and dextroamphetamine are also known as L-amph or levamfetamine (INN) and D-amph or dexamfetamine (INN) respectively.
Jump up ^ The active ingredient in some OTC inhalers in the United States is listed as levmetamfetamine, the INN and USAN of levomethamphetamine.[103][104]
References[edit]
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Jump up ^ "World Drug Report 2015" (PDF).
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Jump up ^ Morton, W. Alexander; Stockton, Gwendolyn G. (8 January 2017). "Methylphenidate Abuse and Psychiatric Side Effects". Primary Care Companion to The Journal of Clinical Psychiatry. 2 (5): 159–164. ISSN 1523-5998. PMC 181133  .
Jump up ^ Treatment, Center for Substance Abuse (1 January 1999). "Chapter 2—How Stimulants Affect the Brain and Behavior". Substance Abuse and Mental Health Services Administration (US).
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^ Jump up to: a b c d e f g h i j k l m Hagel JM, Krizevski R, Marsolais F, Lewinsohn E, Facchini PJ (2012). "Biosynthesis of amphetamine analogs in plants". Trends Plant Sci. 17 (7): 404–412. doi:10.1016/j.tplants.2012.03.004. PMID 22502775. Substituted amphetamines, which are also called phenylpropylamino alkaloids, are a diverse group of nitrogen-containing compounds that feature a phenethylamine backbone with a methyl group at the α-position relative to the nitrogen (Figure 1). Countless variation in functional group substitutions has yielded a collection of synthetic drugs with diverse pharmacological properties as stimulants, empathogens and hallucinogens [3]. ... Beyond (1R,2S)-ephedrine and (1S,2S)-pseudoephedrine, myriad other substituted amphetamines have important pharmaceutical applications. The stereochemistry at the α-carbon is often a key determinant of pharmacological activity, with (S)-enantiomers being more potent. For example, (S)-amphetamine, commonly known as d-amphetamine or dextroamphetamine, displays five times greater psychostimulant activity compared with its (R)-isomer [78]. Most such molecules are produced exclusively through chemical syntheses and many are prescribed widely in modern medicine. For example, (S)-amphetamine (Figure 4b), a key ingredient in Adderall® and Dexedrine®, is used to treat attention deficit hyperactivity disorder (ADHD) [79]. ...
[Figure 4](b) Examples of synthetic, pharmaceutically important substituted amphetamines.
^ Jump up to: a b Glennon RA (2013). "Phenylisopropylamine stimulants: amphetamine-related agents". In Lemke TL, Williams DA, Roche VF, Zito W. Foye's principles of medicinal chemistry (7th ed.). Philadelphia, USA: Wolters Kluwer Health/Lippincott Williams & Wilkins. pp. 646–648. ISBN 9781609133450. Retrieved 11 September 2015. The simplest unsubstituted phenylisopropylamine, 1-phenyl-2-aminopropane, or amphetamine, serves as a common structural template for hallucinogens and psychostimulants. Amphetamine produces central stimulant, anorectic, and sympathomimetic actions, and it is the prototype member of this class (39).
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Jump up ^ Orr K, Taylor D (2007). "Psychostimulants in the Treatment of Depression". CNS Drugs. 21 (3): 239–57. doi:10.2165/00023210-200721030-00004. PMID 17338594.
Jump up ^ Dale, Elena; Bang-Andersen, Benny; Sánchez, Connie (2015). "Emerging mechanisms and treatments for depression beyond SSRIs and SNRIs". Biochemical Pharmacology. 95 (2): 81–97. doi:10.1016/j.bcp.2015.03.011. ISSN 0006-2952. PMID 25813654.
Jump up ^ Efforts of the National Institute on Drug Abuse to Prevent and Treat Prescription Drug Abuse, Testimony Before the Subcommittee on Criminal Justice, Drug Policy, and Human Resources Committee on Government Reform, United States House of Representatives, 26 July 2006
Jump up ^ Docherty, J R (7 January 2017). "Pharmacology of stimulants prohibited by the World Anti-Doping Agency (WADA)". British Journal of Pharmacology. 154 (3): 606–622. doi:10.1038/bjp.2008.124. ISSN 0007-1188. PMC 2439527  .
Jump up ^ Caffeine for the Sustainment of Mental Task Performance: Formulations for Military Operations. Washington (DC):: National Academies Press (US).
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^ Jump up to: a b c Heal DJ, Smith SL, Gosden J, Nutt DJ (June 2013). "Amphetamine, past and present – a pharmacological and clinical perspective". J. Psychopharmacol. 27 (6): 479–496. doi:10.1177/0269881113482532. PMC 3666194  . PMID 23539642.
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^ Jump up to: a b Liddle DG, Connor DJ (June 2013). "Nutritional supplements and ergogenic AIDS". Prim. Care. 40 (2): 487–505. doi:10.1016/j.pop.2013.02.009. PMID 23668655. Amphetamines and caffeine are stimulants that increase alertness, improve focus, decrease reaction time, and delay fatigue, allowing for an increased intensity and duration of training...
Physiologic and performance effects
• Amphetamines increase dopamine/norepinephrine release and inhibit their reuptake, leading to central nervous system (CNS) stimulation
• Amphetamines seem to enhance athletic performance in anaerobic conditions 39 40
• Improved reaction time
• Increased muscle strength and delayed muscle fatigue
• Increased acceleration
• Increased alertness and attention to task
^ Jump up to: a b c Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 318. ISBN 978-0-07-148127-4. Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in individuals with ADHD and in normal subjects...it is now believed that dopamine and norepinephrine, but not serotonin, produce the beneficial effects of stimulants on working memory. At abused (relatively high) doses, stimulants can interfere with working memory and cognitive control, as will be discussed below. It is important to recognize, however, that stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks...through indirect stimulation of dopamine and norepinephrine receptors.
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Although useful in the treatment of ADHD, stimulants are controlled II substances with a history of preclinical and human studies showing potential abuse liability.
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^ Jump up to: a b c Malenka RC, Nestler EJ, Hyman SE (2009). "15". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 370. ISBN 9780071481274. Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons.
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^ Jump up to: a b c d Krasnova IN, Cadet JL (May 2009). "Methamphetamine toxicity and messengers of death". Brain Res. Rev. 60 (2): 379–407. doi:10.1016/j.brainresrev.2009.03.002. PMC 2731235  . PMID 19328213. Neuroimaging studies have revealed that METH can indeed cause neurodegenerative changes in the brains of human addicts (Aron and Paulus, 2007; Chang et al., 2007). These abnormalities include persistent decreases in the levels of dopamine transporters (DAT) in the orbitofrontal cortex, dorsolateral prefrontal cortex, and the caudate-putamen (McCann et al., 1998, 2008; Sekine et al., 2003; Volkow et al., 2001a, 2001c). The density of serotonin transporters (5-HTT) is also decreased in the midbrain, caudate, putamen, hypothalamus, thalamus, the orbitofrontal, temporal, and cingulate cortices of METH-dependent individuals (Sekine et al., 2006) ...
Neuropsychological studies have detected deficits in attention, working memory, and decision-making in chronic METH addicts ...
There is compelling evidence that the negative neuropsychiatric consequences of METH abuse are due, at least in part, to drug-induced neuropathological changes in the brains of these METH-exposed individuals ...
Structural magnetic resonance imaging (MRI) studies in METH addicts have revealed substantial morphological changes in their brains. These include loss of gray matter in the cingulate, limbic, and paralimbic cortices, significant shrinkage of hippocampi, and hypertrophy of white matter (Thompson et al., 2004). In addition, the brains of METH abusers show evidence of hyperintensities in white matter (Bae et al., 2006; Ernst et al., 2000), decreases in the neuronal marker, N-acetylaspartate (Ernst et al., 2000; Sung et al., 2007), reductions in a marker of metabolic integrity, creatine (Sekine et al., 2002) and increases in a marker of glial activation, myoinositol (Chang et al., 2002; Ernst et al., 2000; Sung et al., 2007; Yen et al., 1994). Elevated choline levels, which are indicative of increased cellular membrane synthesis and turnover are also evident in the frontal gray matter of METH abusers (Ernst et al., 2000; Salo et al., 2007; Taylor et al., 2007).
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Jump up ^ "Benzedrex Inhaler Nasal Decongestant Inhaler". B.F. Ascher & Co., Inc. Retrieved 19 December 2013.
Jump up ^ "Proposed Rules". Federal Register. 50 (10): 2226–2227.
Jump up ^ Prince v. Ascher , 90 P.3d 1020 (2004).
Jump up ^ Fornazzari L, Carlen PL, Kapur BM (November 1986). "Intravenous abuse of propylhexedrine (Benzedrex) and the risk of brainstem dysfunction in young adults". Canadian Journal of Neurological Science. 13 (4): 337–9. doi:10.1017/S0317167100036696. PMID 2877725.
Jump up ^ Hunter Gillies; Wayne E. Derman; Timothy D. Noakes; Peter Smith; Alicia Evans & Gary Gabriels (1 December 1996). "Pseudoephedrine is without ergogenic effects during prolonged exercise". Journal of Applied Physiology. 81 (6): 2611–2617. PMID 9018513.
Jump up ^ Hodges, K; Hancock S; Currel K; Hamilton B; Jeukendrup AE (Feb 2006). "Pseudoephedrine enhances performance in 1500-m runners". Medicine and Science in Sports and Exercise. 38 (2): 329–33. doi:10.1249/01.mss.0000183201.79330.9c. PMID 16531903.
Jump up ^ Dickens, Charles (1856) [Digitized 19 February 2010]. "The Orsons of East Africa". Household Words: A Weekly Journal, Volume 14. Bradbury & Evans. p. 176. Retrieved 7 January 2014. (Free eBook)
^ Jump up to: a b Al-Mugahed, Leen (October 2008). "Khat chewing in Yemen: turning over a new leaf – Khat chewing is on the rise in Yemen, raising concerns about the health and social consequences". World Health Organization. Retrieved 8 January 2014.
Jump up ^ Nutt D, King LA, Blakemore C (March 2007). "Development of a rational scale to assess the harm of drugs of potential misuse". Lancet. 369 (9566): 1047–53. doi:10.1016/S0140-6736(07)60464-4. PMID 17382831.
Jump up ^ Haight-Ashbury Free Medical Clinic, Journal of psychoactive drugs, Volume 41, (Haight-Ashbury Publications: 2009), p.3.
Jump up ^ AJ Giannini; WC Price (1986). "Contemporary drugs of abuse". American Family Physician. 33: 207–213.
Jump up ^ Dackis CA, Gold MS (1990). "Addictiveness of central stimulants". Advances in Alcohol & Substance Abuse. 9 (1–2): 9–26. doi:10.1300/J251v09n01_02. PMID 1974121.
Jump up ^ Huskinson, Sally L.; Naylor, Jennifer E.; Rowlett, James K.; Freeman, Kevin B. (7 January 2017). "PREDICTING ABUSE POTENTIAL OF STIMULANTS AND OTHER DOPAMINERGIC DRUGS: OVERVIEW AND RECOMMENDATIONS". Neuropharmacology. 0: 66–80. doi:10.1016/j.neuropharm.2014.03.009. ISSN 0028-3908. PMC 4171344  .
Jump up ^ Stoops, William W. (7 January 2017). "Reinforcing Effects of Stimulants in Humans: Sensitivity of Progressive-Ratio Schedules". Experimental and Clinical Psychopharmacology. 16 (6): 503–512. doi:10.1037/a0013657. ISSN 1064-1297. PMC 2753469  .
Jump up ^ Nutt King, Saulsbury, Blakemore (2007). "Development of a rational scale to assess the harm of drugs of potential misuse". Lancet. 369 (9566): 1047–53. doi:10.1016/S0140-6736(07)60464-4. PMID 17382831. CS1 maint: Multiple names: authors list (link)
Jump up ^ AJ Giannini. Drug Abuse. Los Angeles, Health Information Press, 1999, pp.203–208
External links[edit]
Look up stimulant or upper in Wiktionary, the free dictionary.
Wikimedia Commons has media related to Stimulant.
"Long Island Council on Alcohol & Drug Dependence – About Drugs – Stimulants". Archived from the original on 5 June 2008. Retrieved 4 August 2007. CS1 maint: Unfit url (link)
"Online – Publications – Drugs of Abuse – Stimulants". Archived from the original on 22 September 2006. Retrieved 11 January 2008. CS1 maint: Unfit url (link)
Asia & Pacific Amphetamine-Type Stimulants Information Centre (APAIC)
[show]
v
t
e
Stimulants
Adamantanes
Adapromine
Amantadine
Bromantane
Memantine
Rimantadine
Adenosine antagonists
8-Chlorotheophylline
8-Cyclopentyltheophylline
8-Phenyltheophylline
Aminophylline
Caffeine
CGS-15943
Dimethazan
Paraxanthine
SCH-58261
Theobromine
Theophylline
Alkylamines
Cyclopentamine
Cypenamine
Cyprodenate
Heptaminol
Isometheptene
Levopropylhexedrine
Methylhexaneamine
Octodrine
Propylhexedrine
Tuaminoheptane
Ampakines
CX-516
CX-546
CX-614
CX-691
CX-717
IDRA-21
LY-404,187
LY-503,430
Nooglutyl
Org 26576
PEPA
S-18986
Sunifiram
Unifiram
Arylcyclohexylamines
Benocyclidine
Dieticyclidine
Esketamine
Eticyclidine
Gacyclidine
Ketamine
Phencyclamine
Phencyclidine
Rolicyclidine
Tenocyclidine
Tiletamine
Benzazepines
6-Br-APB
SKF-77434
SKF-81297
SKF-82958
Cholinergics
A-84,543
A-366,833
ABT-202
ABT-418
AR-R17779
Altinicline
Anabasine
Arecoline
Bradanicline
Cotinine
Cytisine
Dianicline
Epibatidine
Epiboxidine
GTS-21
Ispronicline
Nicotine
PHA-543,613
PNU-120,596
PNU-282,987
Pozanicline
Rivanicline
Sazetidine A
SIB-1553A
SSR-180,711
TC-1698
TC-1827
TC-2216
Tebanicline
UB-165
Varenicline
WAY-317,538
Convulsants
Anatoxin-a
Bicuculline
DMCM
Flurothyl
Gabazine
Pentetrazol
Picrotoxin
Strychnine
Thujone
Eugeroics
Adrafinil
Armodafinil
CRL-40,940
CRL-40,941
Fluorenol
JZ-IV-10
Modafinil
Oxazolines
4-Methylaminorex
Aminorex
Clominorex
Cyclazodone
Fenozolone
Fluminorex
Pemoline
Thozalinone
Phenethylamines
1-(4-Methylphenyl)-2-aminobutane
1-Methylamino-1-(3,4-methylenedioxyphenyl)propane
2-Fuoroamphetamine
2-Fuoromethamphetamine
2-OH-PEA
2-Phenyl-3-aminobutane
2,3-MDA
3-Fuoroamphetamine
3-Fluoroethamphetamine
3-Fluoromethcathinone
3-Methoxyamphetamine
3-Methylamphetamine
3,4-DMMC
4-BMC
4-CMC
4-Ethylamphetamine
4-Fluoroamphetamine
4-Fluoromethamphetamine
4-MA
4-Methylbuphedrone
4-Methylcathinone
4-MMA
4-Methylpentedrone
4-MTA
6-FNE
AL-1095
Alfetamine
a-Ethylphenethylamine
Amfecloral
Amfepentorex
Amfepramone
Amidephrine
2-Amino-1,2-dihydronaphthalene
2-Aminoindane
5-(2-Aminopropyl)indole
2-Aminotetralin
Acridorex
Amphetamine (Dextroamphetamine, Levoamphetamine)
Amphetaminil
Arbutamine
β-Methylphenethylamine
β-Phenylmethamphetamine
Benfluorex
Benzedrone
Benzphetamine
BDB
BOH
3-Benzhydrylmorpholine
BPAP
Buphedrone
Bupropion
Butylone
Camfetamine
Cathine
Cathinone
Chlorphentermine
Cilobamine
Cinnamedrine
Clenbuterol
Clobenzorex
Cloforex
Clortermine
Cypenamine
D-Deprenyl
Denopamine
Dimethoxyamphetamine
Dimethylamphetamine
Dimethylcathinone
Dobutamine
DOPA (Dextrodopa, Levodopa)
Dopamine
Dopexamine
Droxidopa
EBDB
Ephedrine
Epinephrine
Epinine
Etafedrine
Ethcathinone
Ethylnorepinephrine
Ethylone
Etilamfetamine
Etilefrine
Famprofazone
Fencamfamin
Fencamine
Fenethylline
Fenfluramine (Dexfenfluramine, Levofenfluramine)
Fenproporex
Feprosidnine
Flephedrone
Fludorex
Formetorex
Furfenorex
Gepefrine
Hexapradol
Hexedrone
HMMA
Hordenine
4-Hydroxyamphetamine
5-Iodo-2-aminoindane
Ibopamine
IMP
Indanylamphetamine
Iofetamine
Isoetarine
Isoethcathinone
Isoprenaline
L-Deprenyl (Selegiline)
Lefetamine
Lisdexamfetamine
Lophophine
MBDB
MDA (tenamfetamine)
MDBU
MDEA
MDMA (midomafetamine)
MDMPEA
MDOH
MDPR
MDPEA
Mefenorex
Mephedrone
Mephentermine
Metanephrine
Metaraminol
Mesocarb
Methamphetamine (Dextromethamphetamine, Levomethamphetamine)
Methoxamine
Methoxyphenamine
MMA
Methcathinone
Methedrone
Methoxyphenamine
Methylenedioxycathinone
Methylone
Mexedrone
MMDA
MMDMA
MMMA
Morforex
N,alpha-Diethylphenylethylamine
N-Ethylbuphedrone
N-Ethylhexedrone
N,N-Dimethylphenethylamine
Naphthylamphetamine
Nisoxetine
Norepinephrine
Norfenefrine
Norfenfluramine
Normetanephrine
L-Norpseudoephedrine
Octopamine (drug)
Orciprenaline
Ortetamine
Oxifentorex
Oxilofrine
PBA
PCA
PCMA
PHA
Pentorex
Pentedrone
Pentylone
Phenatine
Phenpromethamine
Phentermine
Phenylalanine
Phenylephrine
Phenylpropanolamine
Pholedrine
PIA
PMA
PMEA
PMMA
PPAP
Phthalimidopropiophenone
Prenylamine
Propylamphetamine
Pseudoephedrine
Ropinirole
Salbutamol (Levosalbutamol)
Sibutramine
Solriamfetol
Synephrine
Theodrenaline
Tiflorex
Tranylcypromine
Tyramine
Tyrosine
Xylopropamine
Zylofuramine
Phenylmorpholines
3-Fluorophenmetrazine
Fenbutrazate
Fenmetramide
G-130
Manifaxine
Morazone
Morforex
Oxaflozane
PD-128,907
Phendimetrazine
Phenmetrazine
2-Phenyl-3,6-dimethylmorpholine
Pseudophenmetrazine
Radafaxine
Piperazines
2C-B-BZP
3C-PEP
BZP
CM156
DBL-583
GBR-12783
GBR-12935
GBR-13069
GBR-13098
GBR-13119
MeOPP
MBZP
oMPP
Vanoxerine
Piperidines
1-Benzyl-4-(2-(diphenylmethoxy)ethyl)piperidine
2-Benzylpiperidine
2-Methyl-3-phenylpiperidine
3,4-Dichloromethylphenidate
4-Benzylpiperidine
4-Fluoromethylphenidate
4-Methylmethylphenidate
Desoxypipradrol
Difemetorex
Diphenylpyraline
Ethylnaphthidate
Ethylphenidate
Methylnaphthidate
Isopropylphenidate
Methylphenidate (Dexmethylphenidate)
Nocaine
Phacetoperane
Pipradrol
Propylphenidate
SCH-5472
Pyrrolidines
2-Diphenylmethylpyrrolidine
5-DBFPV
α-PPP
α-PBP
α-PHP
α-PVP
α-PVT
Diphenylprolinol
DMPVP
FPOP
FPVP
MDPPP
MDPBP
MPBP
MPHP
MPPP
MOPVP
MOPPP
Indapyrophenidone
MDPV
Naphyrone
PEP
Picilorex
Prolintane
Pyrovalerone
Racetams
Oxiracetam
Phenylpiracetam
Phenylpiracetam hydrazide
Tropanes
4-fluorotropacocaine
4'-Fluorococaine
Altropane (IACFT)
Brasofensine
CFT (WIN 35,428)
β-CIT (RTI-55)
Cocaethylene
Cocaine
Dichloropane (RTI-111)
Difluoropine
FE-β-CPPIT
FP-β-CPPIT
Ioflupane (123I)
Norcocaine
PIT
PTT
RTI-31
RTI-32
RTI-51
RTI-112
RTI-113
RTI-120
RTI-121 (IPCIT)
RTI-126
RTI-150
RTI-177
RTI-229
RTI-336
RTI-354
RTI-371
RTI-386
Salicylmethylecgonine
Tesofensine
Troparil (β-CPT, WIN 35,065-2)
Tropoxane
WF-23
WF-33
Tryptamines
4-HO-αMT
4-Methyl-αET
4-Methyl-αMT
5-Chloro-αMT
5-Fluoro-αMT
5-MeO-αET
5-MeO-αMT
5-MeO-DIPT
6-Fluoro-αMT
7-Methyl-αET
αET
αMT
Others
2-MDP
3,3-Diphenylcyclobutanamine
Amfonelic acid
Amineptine
Amiphenazole
Atipamezole
Atomoxetine
Bemegride
Benzydamine
BTQ
BTS 74,398
Centanafadine
Ciclazindol
Clofenciclan
Cropropamide
Crotetamide
D-161
Desipramine
Diclofensine
Dimethocaine
Efaroxan
Etamivan
Fenisorex
Fenpentadiol
Gamfexine
Gilutensin
GSK1360707F
GYKI-52895
Hexacyclonate
Idazoxan
Indanorex
Indatraline
JNJ-7925476
Lazabemide
Leptacline
Lomevactone
LR-5182
Mazindol
Meclofenoxate
Medifoxamine
Mefexamide
Methamnetamine
Methastyridone
Methiopropamine
Naphthylaminopropane
Nefopam
Nikethamide
Nomifensine
O-2172
Oxaprotiline
PNU-99,194
PRC200-SS
Rasagiline
Rauwolscine
Rubidium chloride
Setazindol
Tametraline
Tandamine
Thiopropamine
Thiothinone
Trazium
UH-232
Yohimbine
ATC code: N06B
[show]
v
t
e
Pharmacology: major drug groups
Gastrointestinal tract/
metabolism (A)
stomach acid
Antacids
H2 antagonists
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Antiemetics
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Muscles, bones,
and joints (M)
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Brain and
nervous system (N)
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system (R)
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H1 antagonists
Sensory organs (S)
Ophthalmologicals
Otologicals
Other ATC (V)
Antidotes
Contrast media
Radiopharmaceuticals
Dressings
Senotherapeutics
[show]
v
t
e
Recreational drug use
Major
recreational
drugs
Depressants
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Freon
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Dilaudid
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Mitragyna speciosa
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Oxycodone
/paracetamol
Tramadol
Stimulants
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Betel
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NDL: 00564760
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