Jump to content

Levoamphetamine

From Wikipedia, the free encyclopedia
(Redirected from Levaphetamine)
Not to be confused with Lisdexamfetamine or Levomethamphetamine.
For the racemate, see Amphetamine.

Levoamphetamine
INN: Levamfetamine
Clinical data
Trade namesCydril, Adderall, Evekeo, Benzedrine, others
Other namesl-Amphetamine, Levamfetamine;[1] Levafetamine; C-105; C105
Routes of
administration		Oral (as part of Adderall, Evekeo, and generic amphetamine sulfate[2][3])
Drug classAmphetamine; Stimulant; Sympathomimetic; Norepinephrine releasing agent; TAAR1 agonist
Legal status
Legal status
Pharmacokinetic data
Protein binding31.7%[4]
MetabolismHydroxylation (CYP2D6), oxidative deamination[3]
MetabolitesL-4-Hydroxyamphetamine[3]
Elimination half-life11.7–15.2 hours[5][3]
ExcretionUrine[6][7]
Identifiers
  • (2R)-1-Phenylpropan-2-amine[8]
CAS Number
PubChem CID
IUPHAR/BPS
ChemSpider
UNII
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.005.320 Edit this at Wikidata
Chemical and physical data
FormulaC9H13N
Molar mass135.210 g·mol−1
3D model (JSmol)
ChiralityLevorotatory enantiomer
  • C[C@@H](N)Cc1ccccc1
  • InChI=1S/C9H13N/c1-8(10)7-9-5-3-2-4-6-9/h2-6,8H,7,10H2,1H3/t8-/m1/s1 checkY
  • Key:KWTSXDURSIMDCE-MRVPVSSYSA-N checkY

Levoamphetamine[note 1] is a stimulant medication which is used in the treatment of certain medical conditions.[10] It was previously marketed by itself under the brand name Cydril, but is now available only in combination with dextroamphetamine in varying ratios under brand names like Adderall and Evekeo.[10][5] The drug is known to increase wakefulness and concentration in association with decreased appetite and fatigue.[11][12] Pharmaceuticals that contain levoamphetamine are currently indicated and prescribed for the treatment of attention deficit hyperactivity disorder (ADHD), obesity, and narcolepsy in some countries.[10][5][13] Levoamphetamine is taken by mouth.[10][5]

Levoamphetamine acts as a releasing agent of the monoamine neurotransmitters norepinephrine and dopamine.[10] It is similar to dextroamphetamine in its ability to release norepinephrine and in its sympathomimetic effects but is a few times weaker than dextroamphetamine in its capacity to release dopamine and in its psychostimulant effects.[10][14][12] Levoamphetamine is the levorotatory stereoisomer of the racemic amphetamine molecule, whereas dextroamphetamine is the dextrorotatory isomer.[10][5]

Levoamphetamine was first introduced in the form of racemic amphetamine under the brand name Benzedrine in 1935 and as an enantiopure drug under the brand name Cydril in the 1970s.[10][15] While pharmaceutical formulations containing enantiopure levoamphetamine are no longer manufactured,[10] levomethamphetamine (levmetamfetamine) is still marketed and sold over-the-counter as a nasal decongestant.[16] In addition to being used in pharmaceutical drugs itself, levoamphetamine is a known active metabolite of certain other drugs, such as selegiline (L-deprenyl).[17][7]

Medical uses

[edit]

Levoamphetamine has been used in the treatment of attention deficit hyperactivity disorder (ADHD) both alone and in combination with dextroamphetamine at different ratios.[10][12] Levoamphetamine on its own has been found to be effective in the treatment of ADHD in multiple clinical studies conducted in the 1970s.[10][12] The clinical dosages and potencies of levoamphetamine and dextroamphetamine in the treatment of ADHD have been fairly similar in these older studies.[10][12]

Available forms

[edit]

Racemic amphetamine

[edit]

The first patented amphetamine brand, Benzedrine, was a racemic (i.e., equal parts) mixture of the free bases or the more stable sulfate salts of both amphetamine enantiomers (levoamphetamine and dextroamphetamine) that was introduced in the United States in 1934 as an inhaler for treating nasal congestion.[2] It was later realized that the amphetamine enantiomers could treat obesity, narcolepsy, and ADHD.[2][3] Because of the greater central nervous system effect of the dextrorotatory enantiomer (i.e., dextroamphetamine), sold as Dexedrine, prescription of the Benzedrine brand fell and was eventually discontinued.[18] However, in 2012, racemic amphetamine sulfate was reintroduced as the Evekeo brand name.[3][19]

Adderall

[edit]

Adderall is a 3.1:1 mixture of dextro- to levo- amphetamine base equivalent pharmaceutical that contains equal amounts (by weight) of four salts: dextroamphetamine sulfate, amphetamine sulfate, dextroamphetamine saccharate and amphetamine (D,L)-aspartate monohydrate. This result is a 76% dextroamphetamine to 24% levoamphetamine, or 3⁄4 to 1⁄4 ratio.[20][21]

Evekeo

[edit]

Evekeo is an FDA-approved medication that contains racemic amphetamine sulfate (i.e., 50% levoamphetamine sulfate and 50% dextroamphetamine sulfate).[3] It is approved for the treatment of narcolepsy, ADHD, and exogenous obesity.[3] The orally disintegrating tablets are approved for the treatment of attention deficit hyperactivity disorder (ADHD) in children and adolescents aged six to 17 years of age.[22]

Other forms

[edit]

Products using amphetamine base are now marketed. Dyanavel XR, a liquid suspension form became available in 2015, and contains about 24% levoamphetamine.[23] Adzenys XR, an orally dissolving tablet came to market in 2016 and contains 25% levoamphetamine.[24][25]

Side effects

[edit]

Levoamphetamine can produce sympathomimetic side effects.[6]

Pharmacology

[edit]

Pharmacodynamics

[edit]
Monoamine release of levoamphetamine and related agents (EC50Tooltip Half maximal effective concentration, nM)
Compound NETooltip Norepinephrine DATooltip Dopamine 5-HTTooltip Serotonin Ref
Phenethylamine 10.9 39.5 >10000 [26][27][28]
Amphetamine ND ND ND ND
  D-Amphetamine 6.6–7.2 5.8–24.8 698–1765 [29][30]
  L-Amphetamine 9.5 27.7 ND [27][28]
Racephedrine ND ND ND ND
  Ephedrine (D-) 43.1–72.4 236–1350 >10000 [29]
  L-Ephedrine 218 2104 >10000 [29][31]
Methamphetamine ND ND ND ND
  D-Methamphetamine 12.3–13.8 8.5–24.5 736–1291.7 [29][32]
  L-Methamphetamine 28.5 416 4640 [29]
Racemic pseudoephedrine ND ND ND ND
  D-Pseudoephedrine 4092 9125 >10000 [31]
  Pseudoephedrine (L-) 224 1988 >10000 [31]
Notes: The smaller the value, the more strongly the drug releases the neurotransmitter. See also Monoamine releasing agent § Activity profiles for a larger table with more compounds. Refs: [33][34]

Levoamphetamine, similarly to dextroamphetamine, acts as a reuptake inhibitor and releasing agent of norepinephrine and dopamine in vitro.[10][14] However, there are differences in potency between the two compounds.[10][14] Levoamphetamine is either similar in potency or somewhat more potent in inducing the release of norepinephrine than dextroamphetamine, whereas dextroamphetamine is approximately 4-fold more potent in inducing the release of dopamine than levoamphetamine.[10] In addition, as a reuptake inhibitor, levoamphetamine is about 3- to 7-fold less potent than dextroamphetamine in inhibiting dopamine reuptake but is only about 2-fold less potent in inhibiting norepinephrine reuptake.[10] Dextroamphetamine is very weak as a reuptake inhibitor of serotonin, whereas levoamphetamine is essentially inactive in this regard.[10] Levoamphetamine and dextroamphetamine are both also relatively weak reversible inhibitors of monoamine oxidase (MAO) and hence can inhibit catecholamine metabolism.[10][35][36][37] However, this action may not occur significantly at clinical doses and may only be relevant to high doses.[35]

In rodent studies, both dextroamphetamine and levoamphetamine dose-dependently induce the release of dopamine in the striatum and norepinephrine in the prefrontal cortex.[10] Dextroamphetamine is about 3- to 5-fold more potent in increasing striatal dopamine levels as levoamphetamine in rodents in vivo, whereas the two enantiomers are about equally effective in terms of increasing prefrontal norepinephrine levels.[10] Dextroamphetamine has greater effects on dopamine levels than on norepinephrine levels, whereas levoamphetamine has relatively more balanced effects on dopamine and norepinephrine levels.[10] As with rodent studies, levoamphetamine and dextroamphetamine have been found to be similarly potent in elevating norepinephrine levels in cerebrospinal fluid in monkeys.[38][39] By an uncertain mechanism, the striatal dopamine release of dextroamphetamine in rodents appears to be prolonged by levoamphetamine when the two enantiomers are administered at a 3:1 ratio (though not at a 1:1 ratio).[10]

The catecholamine-releasing effects of levoamphetamine and dextroamphetamine in rodents have a fast onset of action, with a peak of effect after about 30 to 45 minutes, are large in magnitude (e.g., 700–1,500% of baseline for dopamine and 400–450% of baseline for norepinephrine), and decline relatively rapidly after the effects reach their maximum.[10] The magnitudes of the effects of amphetamines are greater than those of classical reuptake inhibitors like atomoxetine and bupropion.[10] In addition, unlike with reuptake inhibitors, there is no dose–effect ceiling in the case of amphetamines.[10] Although dextroamphetamine is more potent than levoamphetamine, both enantiomers can maximally increase striatal dopamine release by more than 5,000% of baseline.[10][40] This is in contrast to reuptake inhibitors like bupropion and vanoxerine, which have 5- to 10-fold smaller maximal impacts on dopamine levels and, in contrast to amphetamines, were not experienced as stimulating or euphoric.[10]

Dextroamphetamine has greater potency in producing stimulant-like effects in rodents and non-human primates than levoamphetamine.[10] Some rodent studies have found it to be 5- to 10-fold more potent in its stimulant-like effects than levoamphetamine.[14][41][42] Levoamphetamine is also less potent than dextroamphetamine in its anorectic effects in rodents.[14][43] Dextroamphetamine is about 4-fold more potent than levoamphetamine in motivating self-administration in monkeys and is about 2- to 3-fold more potent than levoamphetamine in terms of positive reinforcing effects in humans.[10][7][44] Potency ratios of dextroamphetamine versus levoamphetamine with single doses of 5 to 80 mg in terms of psychological effects in humans including stimulation, wakefulness, activation, euphoria, reduction of hyperactivity, and exacerbation of psychosis have ranged from 1:1 to 4:1 in a variety of older clinical studies.[12][note 2][45] With very large doses, ranging from 270 to 640 mg, the potency ratios of dextroamphetamine and levoamphetamine in stimulating locomotor activity and inducing amphetamine psychosis in humans have ranged from 1:1 to 2:1 in a couple studies.[12] The differences in potency and dopamine versus norepinephrine release between dextroamphetamine and levoamphetamine are suggestive of dopamine being the primary neurochemical mediator responsible for the stimulant and euphoric effects of these agents.[10]

In addition to inducing norepinephrine release in the brain, levoamphetamine and dextroamphetamine induce the release of epinephrine (adrenaline) in the peripheral sympathetic nervous system and this is related to their cardiovascular effects.[10] Although levoamphetamine is less potent than dextroamphetamine as a stimulant, it is approximately equipotent with dextroamphetamine in producing various peripheral effects, including vasoconstriction, vasopression, and other cardiovascular effects.[14]

Similarly to dextroamphetamine, levoamphetamine has been found to improve symptoms in an animal model of ADHD, the spontaneously hypertensive rat (SHR), including improving sustained attention and reducing overactivity and impulsivity.[46][47][48][49] These findings parallel the clinical results in which both levoamphetamine and dextroamphetamine have been found to be effective in the treatment of ADHD in humans.[10][12]

Unlike the case of dextroamphetamine versus dextromethamphetamine, in which the latter is more effective than the former, levoamphetamine is substantially more potent as a dopamine releaser and stimulant than levomethamphetamine.[35][50] Conversely, levoamphetamine, levomethamphetamine, and dextroamphetamine are all similar in their potencies as norepinephrine releasers.[35][50]

In addition to its catecholamine-releasing activity, levoamphetamine is also an agonist of the trace amine-associated receptor 1 (TAAR1).[51][52] Levoamphetamine has also been found to act as a catecholaminergic activity enhancer (CAE), notably at much lower concentrations than its catecholamine releasing activity.[53][54][55][56] It is similarly potent to selegiline and levomethamphetamine but is more potent than dextromethamphetamine and dextroamphetamine in this action.[55] The CAE effects of such agents may be mediated by TAAR1 agonism.[57][56]

Pharmacokinetics

[edit]

The pharmacokinetics of levoamphetamine have been studied.[5][3] Usually this has been orally in combination with dextroamphetamine at different ratios.[5][3] The pharmacokinetics of levoamphetamine have also been studied as a metabolite of selegiline.[7][17]

Absorption

[edit]

The oral bioavailability of levoamphetamine has been found to be similar to that of dextroamphetamine.[58]

The time to peak levels of levoamphetamine with immediate-release (IR) formulations of amphetamine ranges from 2.5 to 3.5 hours and with extended-release (ER) formulations ranges from 5.3 to 8.2 hours depending on the formulation and the study.[5][58] For comparison, the time to peak levels of dextroamphetamine with IR formulations ranges from 2.4 to 3.3 hours and with ER formulations ranges from 4.0 to 8.0 hours.[5][58] The peak levels of levoamphetamine are proportionally similar to those of dextroamphetamine with administration of amphetamine at varying ratios.[5] With a single oral dose of 10 mg racemic amphetamine (a 1:1 ratio of enantiomers, or 5 mg dextroamphetamine and 5 mg levoamphetamine), peak levels of dextroamphetamine were 14.7 ng/mL and peak levels of levoamphetamine were 12.0 ng/mL in one study.[5]

Food does not affect the peak levels or overall exposure to levoamphetamine or dextroamphetamine with IR racemic amphetamine.[3] However, time to peak levels was delayed from 2.5 hours (range 1.5–6 hours) to 4.5 hours (range 2.5–8.0 hours).[3]

During oral selegiline therapy at a dosage of 10 mg/day, circulating levels of levoamphetamine have been found to be 6 to 8 ng/mL and levels of levomethamphetamine have been reported to be 9 to 14 ng/mL.[7] Although levels of levoamphetamine and levomethamphetamine are relatively low at typical doses of selegiline, they could be clinically relevant and may contribute to the effects and side effects of selegiline.[7]

Distribution

[edit]

The volume of distribution of both levoamphetamine and dextroamphetamine is about 3 to 4 L/kg.[58]

The plasma protein binding of levoamphetamine is 31.7%, whereas that of dextroamphetamine was 29.0% in the same study.[4]

Metabolism

[edit]

Levoamphetamine and dextroamphetamine are metabolized via CYP2D6-mediated hydroxylation to produce 4-hydroxyamphetamine and additionally via oxidative deamination.[3] There are several enzymes involved in the metabolism of amphetamine, of which CYP2D6 is one.[3] Levoamphetamine seems to be metabolized somewhat less efficiently than dextroamphetamine.[58]

The pharmacokinetics of levoamphetamine generated as a metabolite from selegiline have been found not to significantly vary in CYP2D6 poor metabolizers versus extensive metabolizers, suggesting that CYP2D6 may be minimally involved in the clinical metabolism of levoamphetamine.[17][59]

Elimination

[edit]

The mean elimination half-life of levoamphetamine ranges from 11.7 to 15.2 hours in different studies.[5][58][3] Its half-life is somewhat longer than that of dextroamphetamine, with a difference of about 1 to 2 hours.[5][6][58] For comparison, in the same studies that reported the preceding values for levoamphetamine's half-life, the half-life of dextroamphetamine ranged from 10.0 to 12.4 hours.[5][58][3]

The elimination of amphetamine is highly dependent on urinary pH.[3][6] Urinary acidifying agents like ascorbic acid and ammonium chloride increase amphetamine excretion and reduce its elimination half-life, whereas urinary alkalinizing agents like acetazolamide enhance renal tubular reabsorption and extend its half-life.[6] The urinary excretion of unchanged amphetamine is 70% on average with a urinary pH of 6.6 and 17 to 43% at a urinary pH of greater than 6.7.[3]

With selegiline at an oral dose of 10 mg, levoamphetamine and levomethamphetamine are eliminated in urine and recovery of levoamphetamine is 9 to 30% (or about 1–3 mg) while that of levomethamphetamine is 20 to 60% (or about 2–6 mg).[7]

Chemistry

[edit]

Levoamphetamine is a substituted phenethylamine and amphetamine. It is also known as L-α-methyl-β-phenylethylamine or as (2R)-1-phenylpropan-2-amine.[8] Levoamphetamine is the levorotatory stereoisomer of the amphetamine molecule. Racemic amphetamine contains two optical isomers in equal amounts, dextroamphetamine (the dextrorotatory enantiomer) and levoamphetamine.[20][21]

History

[edit]

The origin of the amphetamine psychostimulants comes from ephedra.[60] This plant, also known as "ma huang", is an herb which has been used for thousands of years in traditional Chinese medicine as a stimulant and antiasthmatic medicine.[61][62] Ephedrine ((1R,2S)-β-hydroxy-N-methylamphetamine), an analogue and derivative of amphetamine and the major pharmacologically active constituent of ephedra, was first isolated from the plant in 1885.[63][60] Another plant, known as Catha edulis (khat), also naturally contains amphetamines, specifically cathine ((1S,2S)-β-hydroxyamphetamine) and cathinone (β-ketoamphetamine).[62][64] It has a long history of use for its stimulant effects in Eastern Africa and the Arabian Peninsula.[62][64] However, cathine was not isolated from khat until 1930 and cathinone was not isolated from the plant until 1975.[64]

Amphetamine, which is a racemic mixture of dextroamphetamine and levoamphetamine, was first discovered in 1887, shortly after the isolation of ephedrine.[65][60] However, it was not until 1927 that amphetamine was synthesized by Gordon Alles and was studied by him in animals and humans.[10] This led to the discovery of the stimulating effects of amphetamine in humans in 1929 after Alles injected himself with 50 mg of the drug.[65][10] Levoamphetamine was first introduced in the form of racemic amphetamine (a 1:1 combination of levoamphetamine and dextroamphetamine) under the brand name Benzedrine in 1935.[10] It was indicated for the treatment of narcolepsy, mild depression, parkinsonism, and a variety of other conditions.[10] Dextroamphetamine was found to be the more potent of the two enantiomers of amphetamine and was introduced as an enantiopure drug under the brand name Dexedrine in 1937.[10] Consequent to its lower potency, levoamphetamine has received far less attention than racemic amphetamine or dextroamphetamine.[10]

Levoamphetamine was studied in the treatment of attention deficit hyperactivity disorder (ADHD) in the 1970s and was found to be clinically effective for this condition similarly to dextroamphetamine.[10] As a result, it was marketed as an enantiopure drug under the brand name Cydril for the treatment of ADHD in the 1970s.[10][15] However, it was reported in 1976 that racemic amphetamine was less effective than dextroamphetamine in treating ADHD.[10] As a result of this study, use of racemic amphetamine in the treatment of ADHD dramatically declined in favor of dextroamphetamine.[10] Enantiopure levoamphetamine was eventually discontinued and is no longer available today.[10]

Society and culture

[edit]

Recreational use

[edit]

Misuse of enantiopure levoamphetamine and levomethamphetamine is reportedly not known.[17] However, rare cases of misuse of levomethamphetamine, which is available over-the-counter as a nasal decongestant, actually have been reported.[66][67][68][69] Due to their lower efficacy in stimulating dopamine release and their reduced potency as psychostimulants, levoamphetamine and levomethamphetamine would theoretically be expected to have less misuse potential than the corresponding dextroamphetamine and dextromethamphetamine forms.[17]

Research

[edit]

Levoamphetamine as an enantiopure drug has been studied in the past in a variety of contexts.[11] These include its effects in and/or treatment of mood,[11] "minimal brain dysfunction",[70] narcolepsy,[11][71] "hyperkinetic syndrome" and aggression,[72][15] sleep,[73][74] schizophrenia,[75] wakefulness,[76] Tourette's syndrome,[77] and Parkinson's disease, among others.[11][78] Levoamphetamine has been studied in the treatment of multiple sclerosis in more modern studies and has been reported to improve cognition and memory in this condition as well.[79][80][81][82][83][84] It was under development for this indication under the name levafetamine and the developmental code name C-105 and reached phase 2 clinical trials, but development was discontinued sometime after 2008.[85]

Other drugs

[edit]

Selegiline

[edit]
Main article: Selegiline

Levoamphetamine is a major active metabolite of selegiline (L-deprenyl; N-propargyl-L-methamphetamine).[7][86] Selegiline is a monoamine oxidase inhibitor (MAOI), specifically a selective inhibitor of monoamine oxidase B (MAO-B) at lower doses and a dual inhibitor of both monoamine oxidase A (MAO-A) and MAO-B at higher doses.[7][87] It also has additional activities, such as acting as a catecholaminergic activity enhancer (CAE), possibly via agonism of the TAAR1, and having potential neuroprotective effects.[88][87][56] Selegiline is clinically used as an antiparkinsonian agent in the treatment of Parkinson's disease and as an antidepressant in the treatment of major depressive disorder.[88][87]

In addition to levoamphetamine, selegiline also metabolizes into levomethamphetamine.[86][7] With a 10 mg oral dose of selegiline, about 2 to 6 mg levomethamphetamine and 1 to 3 mg levoamphetamine is excreted in urine.[7][89][86][90] As levoamphetamine and levomethamphetamine are norepinephrine and/or dopamine releasing agents, they may contribute to the effects and side effects of selegiline.[91][92][33] This may particularly include cardiovascular and sympathomimetic effects of selegiline.[91][93][94][95] Other selective MAO-B inhibitors that do not metabolize into amphetamine metabolites or have associated cardiovascular effects, such as rasagiline, have also been developed and introduced.[91][96]

Because selegiline metabolizes into levoamphetamine and levomethamphetamine, people taking selegiline can erroneously test positive for amphetamines on drug tests.[97][98]

Notes

[edit]
  1. ^ Synonyms and alternate spellings include: (2R)-1-phenylpropan-2-amine (IUPAC name), levamfetamine (International Nonproprietary Name [INN]), (R)-amphetamine, (−)-amphetamine, l-amphetamine, and L-amphetamine.[8][9]
  2. ^ Smith & Davis (1977) reviewed 11 clinical studies of dextroamphetamine and levoamphetamine including doses and potency ratios in terms of a variety of psychological and behavioral effects.[12] The summaries of these studies are in Table 1 of the paper.[12]

References

[edit]
  1. ^ CID 32893 from PubChem
  2. ^ 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.
  3. ^ a b c d e f g h i j k l m n o p q r "Evekeo- amphetamine sulfate tablet". DailyMed. 14 August 2019. Retrieved 7 April 2020.
  4. ^ a b Losacker M, Roehrich J, Hess C (October 2021). "Enantioselective determination of plasma protein binding of common amphetamine-type stimulants". J Pharm Biomed Anal. 205: 114317. doi:10.1016/j.jpba.2021.114317. PMID 34419812.
  5. ^ a b c d e f g h i j k l m n Markowitz JS, Patrick KS (October 2017). "The Clinical Pharmacokinetics of Amphetamines Utilized in the Treatment of Attention-Deficit/Hyperactivity Disorder". J Child Adolesc Psychopharmacol. 27 (8): 678–689. doi:10.1089/cap.2017.0071. PMID 28910145.
  6. ^ a b c d e Patrick KS, Markowitz JS (1997). "Pharmacology of methylphenidate, amphetamine enantiomers and pemoline in attention-deficit hyperactivity disorder". Human Psychopharmacology: Clinical and Experimental. 12 (6): 527–546. doi:10.1002/(SICI)1099-1077(199711/12)12:6<527::AID-HUP932>3.0.CO;2-U. ISSN 0885-6222.
  7. ^ a b c d e f g h i j k Heinonen EH, Lammintausta R (1991). "A review of the pharmacology of selegiline". Acta Neurol Scand Suppl. 136: 44–59. doi:10.1111/j.1600-0404.1991.tb05020.x. PMID 1686954.
  8. ^ a b c "L-Amphetamine". PubChem Compound. United States National Library of Medicine – National Center for Biotechnology Information. 30 December 2017. Retrieved 2 January 2018.
  9. ^ "R(-)amphetamine". IUPHAR/BPS Guide to Pharmacology. International Union of Basic and Clinical Pharmacology. Retrieved 2 January 2018.
  10. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq 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.
  11. ^ a b c d e Silverstone T, Wells B (1980). "Clinical Psychopharmacology of Amphetamine and Related Compounds". Amphetamines and Related Stimulants: Chemical, Biological, Clinical, and Sociological Aspects. CRC Press. pp. 147–160. doi:10.1201/9780429279843-10. ISBN 978-0-429-27984-3.
  12. ^ a b c d e f g h i j Smith RC, Davis JM (June 1977). "Comparative effects of d-amphetamine, l-amphetamine, and methylphenidate on mood in man". Psychopharmacology (Berl). 53 (1): 1–12. doi:10.1007/BF00426687. PMID 407607.
  13. ^ Simola N, Carta M (2016). "Amphetamine Usage, Misuse, and Addiction Processes". Neuropathology of Drug Addictions and Substance Misuse. Elsevier. pp. 14–24. doi:10.1016/b978-0-12-800212-4.00002-9. ISBN 978-0-12-800212-4.
  14. ^ a b c d e f Biel JH, Bopp BA (1978). "Amphetamines: Structure-Activity Relationships". Stimulants. Boston, MA: Springer US. pp. 1–39. doi:10.1007/978-1-4757-0510-2_1. ISBN 978-1-4757-0512-6.
  15. ^ a b c Arnold LE, Wender PH, McCloskey K, Snyder SH (December 1972). "Levoamphetamine and dextroamphetamine: comparative efficacy in the hyperkinetic syndrome. Assessment by target symptoms". Arch Gen Psychiatry. 27 (6): 816–22. doi:10.1001/archpsyc.1972.01750300078015. PMID 4564954.
  16. ^ Barkholtz HM, Hadzima R, Miles A (July 2023). "Pharmacology of R-(-)-Methamphetamine in Humans: A Systematic Review of the Literature". ACS Pharmacol Transl Sci. 6 (7): 914–924. doi:10.1021/acsptsci.3c00019. PMC 10353062. PMID 37470013.
  17. ^ a b c d e Kraemer T, Maurer HH (April 2002). "Toxicokinetics of amphetamines: metabolism and toxicokinetic data of designer drugs, amphetamine, methamphetamine, and their N-alkyl derivatives". Ther Drug Monit. 24 (2): 277–89. doi:10.1097/00007691-200204000-00009. PMID 11897973.
  18. ^ "Benzedrine: FDA-Approved Drugs". U.S. Food and Drug Administration (FDA). Retrieved 4 September 2015.
  19. ^ "Evekeo: FDA-Approved Drugs". U.S. Food and Drug Administration (FDA). Retrieved 11 August 2015.
  20. ^ a b "Adderall XR- dextroamphetamine sulfate, dextroamphetamine saccharate, amphetamine sulfate and amphetamine aspartate capsule, extended release". DailyMed. 17 July 2019. Retrieved 7 April 2020.
  21. ^ a b "Adderall- dextroamphetamine saccharate, amphetamine aspartate, dextroamphetamine sulfate, and amphetamine sulfate tablet". DailyMed. 8 November 2019. Retrieved 7 April 2020.
  22. ^ "Evekeo ODT- amphetamine sulfate tablet, orally disintegrating". DailyMed. 20 February 2020. Retrieved 7 April 2020.
  23. ^ "Dyanavel XR Prescribing Information". January 2017. Retrieved 14 May 2017.
  24. ^ "Adzenys XR-ODT- amphetamine tablet, orally disintegrating". DailyMed. 22 January 2020. Retrieved 7 April 2020.
  25. ^ "Adzenys ER- amphetamine suspension, extended release". DailyMed. 21 January 2020. Retrieved 7 April 2020.
  26. ^ Reith ME, Blough BE, Hong WC, Jones KT, Schmitt KC, Baumann MH, et al. (February 2015). "Behavioral, biological, and chemical perspectives on atypical agents targeting the dopamine transporter". Drug and Alcohol Dependence. 147: 1–19. doi:10.1016/j.drugalcdep.2014.12.005. PMC 4297708. PMID 25548026.
  27. ^ a b Forsyth AN (22 May 2012). "Synthesis and Biological Evaluation of Rigid Analogues of Methamphetamines". ScholarWorks@UNO. Retrieved 4 November 2024.
  28. ^ a b Blough B (July 2008). "Dopamine-releasing agents". Dopamine Transporters: Chemistry, Biology and Pharmacology. Hoboken [NJ]: Wiley. pp. 305–320. ISBN 978-0-470-11790-3. Archived from the original on 4 November 2024. TABLE 11-2 Comparison of the DAT- and NET-Releasing Activity of a Series of Amphetamines [...]
  29. ^ a b c d e Rothman RB, Baumann MH, Dersch CM, Romero DV, Rice KC, Carroll FI, et al. (January 2001). "Amphetamine-type central nervous system stimulants release norepinephrine more potently than they release dopamine and serotonin". Synapse. 39 (1): 32–41. doi:10.1002/1098-2396(20010101)39:1<32::AID-SYN5>3.0.CO;2-3. PMID 11071707. S2CID 15573624.
  30. ^ Baumann MH, Partilla JS, Lehner KR, Thorndike EB, Hoffman AF, Holy M, et al. (2013). "Powerful cocaine-like actions of 3,4-methylenedioxypyrovalerone (MDPV), a principal constituent of psychoactive 'bath salts' products". Neuropsychopharmacology. 38 (4): 552–562. doi:10.1038/npp.2012.204. PMC 3572453. PMID 23072836.
  31. ^ a b c Rothman RB, Vu N, Partilla JS, Roth BL, Hufeisen SJ, Compton-Toth BA, et al. (2003). "In vitro characterization of ephedrine-related stereoisomers at biogenic amine transporters and the receptorome reveals selective actions as norepinephrine transporter substrates". J. Pharmacol. Exp. Ther. 307 (1): 138–45. doi:10.1124/jpet.103.053975. PMID 12954796. S2CID 19015584.
  32. ^ Baumann MH, Ayestas MA, Partilla JS, Sink JR, Shulgin AT, Daley PF, et al. (2012). "The designer methcathinone analogs, mephedrone and methylone, are substrates for monoamine transporters in brain tissue". Neuropsychopharmacology. 37 (5): 1192–1203. doi:10.1038/npp.2011.304. PMC 3306880. PMID 22169943.
  33. ^ a b Rothman RB, Baumann MH (October 2003). "Monoamine transporters and psychostimulant drugs". Eur J Pharmacol. 479 (1–3): 23–40. doi:10.1016/j.ejphar.2003.08.054. PMID 14612135.
  34. ^ Rothman RB, Baumann MH (2006). "Therapeutic potential of monoamine transporter substrates". Current Topics in Medicinal Chemistry. 6 (17): 1845–1859. doi:10.2174/156802606778249766. PMID 17017961.
  35. ^ a b c d Nishino S, Kotorii N (2016). "Modes of Action of Drugs Related to Narcolepsy: Pharmacology of Wake-Promoting Compounds and Anticataplectics". Narcolepsy: A Clinical Guide (2 ed.). Cham: Springer International Publishing. pp. 307–329. doi:10.1007/978-3-319-23739-8_22. ISBN 978-3-319-23738-1.
  36. ^ Clarke D (1980). "Amphetamine and monoamine oxidase inhibition: an old idea gains new acceptance". Trends in Pharmacological Sciences. 1 (2): 312–313. doi:10.1016/0165-6147(80)90032-2.
  37. ^ Miller HH, Clarke DE (1978). "In vitro inhibition of monoamine oxidase types A and B by d- and l-amphetamine". Communications in Psychopharmacology. 2 (4): 319–325. PMID 729356.
  38. ^ Ziegler MG (1989). "Catecholamine Measurement in Behavioral Research". Handbook of Research Methods in Cardiovascular Behavioral Medicine. Boston, MA: Springer US. pp. 167–183. doi:10.1007/978-1-4899-0906-0_11. ISBN 978-1-4899-0908-4.
  39. ^ Ziegler MG, Lake CR, Ebert MH (August 1979). "Norepinephrine elevations in cerebrospinal fluid after d- and l-amphetamine". European Journal of Pharmacology. 57 (2–3): 127–133. doi:10.1016/0014-2999(79)90358-3. PMID 114399.
  40. ^ Cheetham SC, Kulkarni RS, Rowley HL, Heal DJ (2007). The SH rat model of ADHD has profoundly different catecholaminergic responses to amphetamine's enantiomers compared with Sprague-Dawleys. Neuroscience 2007, San Diego, CA, Nov 3-7, 2007. Society for Neuroscience. Archived from the original on 27 July 2024. Both d- and l-[amphetamine (AMP)] evoked rapid increases in extraneuronal concentrations of [noradrenaline (NA)] and [dopamine (DA)] that reached a maximum 30 or 60 min after administration. However, the [spontaneously hypertensive rats (SHRs)] were much more responsive to AMP's enantiomers than the [Sprague-Dawleys (SDs)]. Thus, 3 mg/kg d-AMP produced a peak increase in [prefrontal cortex (PFC)] NA of 649 ± 87% (p<0.001) in SHRs compared with 198 ± 39% (p<0.05) in SDs; the corresponding figures for [striatal (STR)] DA were 4898 ± 1912% (p<0.001) versus 1606 ± 391% (p<0.001). At 9 mg/kg, l-AMP maximally increased NA efflux by 1069 ± 105% (p<0.001) in SHRs compared with 157 ± 24% (p<0.01) in SDs; the DA figures were 3294 ± 691% (p<0.001) versus 459 ± 107% (p<0.001).
  41. ^ Segal DS (October 1975). "Behavioral characterization of d- and l-amphetamine: neurochemical implications". Science. 190 (4213): 475–477. Bibcode:1975Sci...190..475S. doi:10.1126/science.1166317. PMID 1166317.
  42. ^ Taylor KM, Snyder SH (June 1970). "Amphetamine: differentiation by d and l isomers of behavior involving brain norepinephrine or dopamine". Science. 168 (3938): 1487–1489. Bibcode:1970Sci...168.1487T. doi:10.1126/science.168.3938.1487. PMID 5463064.
  43. ^ Lawlor RB, Trivedi MC, Yelnosky J (June 1969). "A determination of the anorexigenic potential of dl-amphetamine, d-amphetamine, l-amphetamine and phentermine". Arch Int Pharmacodyn Ther. 179 (2): 401–407. PMID 5367311.
  44. ^ Balster RL, Schuster CR (1973). "A comparison of d-amphetamine, l-amphetamine, and methamphetamine self-administration in rhesus monkeys". Pharmacol Biochem Behav. 1 (1): 67–71. doi:10.1016/0091-3057(73)90057-9. PMID 4204513.
  45. ^ Van Kammen DP, Murphy DL (November 1975). "Attenuation of the euphoriant and activating effects of d- and l-amphetamine by lithium carbonate treatment". Psychopharmacologia. 44 (3): 215–224. doi:10.1007/BF00428897. PMID 1824.
  46. ^ Kantak KM (May 2022). "Rodent models of attention-deficit hyperactivity disorder: An updated framework for model validation and therapeutic drug discovery". Pharmacol Biochem Behav. 216: 173378. doi:10.1016/j.pbb.2022.173378. PMID 35367465.
  47. ^ Teal LB, Ingram SM, Bubser M, McClure E, Jones CK (2023). "The Evolving Role of Animal Models in the Discovery and Development of Novel Treatments for Psychiatric Disorders". Drug Development in Psychiatry. Advances in Neurobiology. Vol. 30. Cham: Springer International Publishing. pp. 37–99. doi:10.1007/978-3-031-21054-9_3. ISBN 978-3-031-21053-2. PMID 36928846.
  48. ^ Sagvolden T (March 2011). "Impulsiveness, overactivity, and poorer sustained attention improve by chronic treatment with low doses of l-amphetamine in an animal model of Attention-Deficit/Hyperactivity Disorder (ADHD)". Behav Brain Funct. 7: 6. doi:10.1186/1744-9081-7-6. PMC 3086861. PMID 21450079.
  49. ^ Sagvolden T, Xu T (January 2008). "l-Amphetamine improves poor sustained attention while d-amphetamine reduces overactivity and impulsiveness as well as improves sustained attention in an animal model of Attention-Deficit/Hyperactivity Disorder (ADHD)". Behav Brain Funct. 4: 3. doi:10.1186/1744-9081-4-3. PMC 2265273. PMID 18215285.
  50. ^ a b Kuczenski R, Segal DS, Cho AK, Melega W (February 1995). "Hippocampus norepinephrine, caudate dopamine and serotonin, and behavioral responses to the stereoisomers of amphetamine and methamphetamine". J Neurosci. 15 (2): 1308–1317. doi:10.1523/JNEUROSCI.15-02-01308.1995. PMC 6577819. PMID 7869099.
  51. ^ Sotnikova TD, Caron MG, Gainetdinov RR (August 2009). "Trace amine-associated receptors as emerging therapeutic targets". Mol Pharmacol. 76 (2): 229–35. doi:10.1124/mol.109.055970. PMC 2713119. PMID 19389919. Intriguingly, d- and l-amphetamine, methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA), and other closely related compounds are also able to activate TAAR1 receptors in vitro as evidenced by cAMP stimulation in human embryonic kidney cells.
  52. ^ Reese EA, Norimatsu Y, Grandy MS, Suchland KL, Bunzow JR, Grandy DK (January 2014). "Exploring the determinants of trace amine-associated receptor 1's functional selectivity for the stereoisomers of amphetamine and methamphetamine". J Med Chem. 57 (2): 378–390. doi:10.1021/jm401316v. PMID 24354319.
  53. ^ Knoll J (2001). "Antiaging compounds: (-)deprenyl (selegeline) and (-)1-(benzofuran-2-yl)-2-propylaminopentane, [(-)BPAP], a selective highly potent enhancer of the impulse propagation mediated release of catecholamine and serotonin in the brain". CNS Drug Rev. 7 (3): 317–45. doi:10.1111/j.1527-3458.2001.tb00202.x. PMC 6494119. PMID 11607046.
  54. ^ Knoll J (February 1998). "(-)Deprenyl (selegiline), a catecholaminergic activity enhancer (CAE) substance acting in the brain". Pharmacol Toxicol. 82 (2): 57–66. doi:10.1111/j.1600-0773.1998.tb01399.x. PMID 9498233.
  55. ^ a b Knoll J, Miklya I (1994). "Multiple, small dose administration of (-)deprenyl enhances catecholaminergic activity and diminishes serotoninergic activity in the brain and these effects are unrelated to MAO-B inhibition". Arch Int Pharmacodyn Ther. 328 (1): 1–15. PMID 7893186.
  56. ^ a b c Harsing LG, Timar J, Miklya I (August 2023). "Striking Neurochemical and Behavioral Differences in the Mode of Action of Selegiline and Rasagiline". Int J Mol Sci. 24 (17): 13334. doi:10.3390/ijms241713334. PMC 10487936. PMID 37686140.
  57. ^ Harsing LG, Knoll J, Miklya I (August 2022). "Enhancer Regulation of Dopaminergic Neurochemical Transmission in the Striatum". Int J Mol Sci. 23 (15): 8543. doi:10.3390/ijms23158543. PMC 9369307. PMID 35955676.
  58. ^ a b c d e f g h Markowitz JS, Melchert PW (July 2022). "The Pharmacokinetics and Pharmacogenomics of Psychostimulants". Child Adolesc Psychiatr Clin N Am. 31 (3): 393–416. doi:10.1016/j.chc.2022.03.003. PMID 35697392.
  59. ^ Scheinin H, Anttila M, Dahl ML, Karnani H, Nyman L, Taavitsainen P, et al. (October 1998). "CYP2D6 polymorphism is not crucial for the disposition of selegiline". Clin Pharmacol Ther. 64 (4): 402–411. doi:10.1016/S0009-9236(98)90071-6. PMID 9797797.
  60. ^ a b c Morelli M, Tognotti E (August 2021). "Brief history of the medical and non-medical use of amphetamine-like psychostimulants". Exp Neurol. 342: 113754. doi:10.1016/j.expneurol.2021.113754. PMID 34000249.
  61. ^ Abourashed EA, El-Alfy AT, Khan IA, Walker L (August 2003). "Ephedra in perspective--a current review". Phytother Res. 17 (7): 703–712. doi:10.1002/ptr.1337. PMID 12916063.
  62. ^ a b c Kalix P (April 1991). "The pharmacology of psychoactive alkaloids from ephedra and catha". J Ethnopharmacol. 32 (1–3): 201–208. doi:10.1016/0378-8741(91)90119-x. PMID 1881158.
  63. ^ Aaron CK (August 1990). "Sympathomimetics". Emerg Med Clin North Am. 8 (3): 513–526. doi:10.1016/S0733-8627(20)30256-X. PMID 2201518.
  64. ^ a b c Patel NB (June 2000). "Mechanism of action of cathinone: the active ingredient of khat (Catha edulis)". East Afr Med J. 77 (6): 329–332. doi:10.4314/eamj.v77i6.46651. PMID 12858935.
  65. ^ a b Rasmussen N (2015). "Amphetamine-Type Stimulants: The Early History of Their Medical and Non-Medical Uses". Int Rev Neurobiol. 120: 9–25. doi:10.1016/bs.irn.2015.02.001. PMID 26070751.
  66. ^ Mendelson JE, McGlothlin D, Harris DS, Foster E, Everhart T, Jacob P, et al. (July 2008). "The clinical pharmacology of intranasal l-methamphetamine". BMC Clin Pharmacol. 8: 4. doi:10.1186/1472-6904-8-4. PMC 2496900. PMID 18644153.
  67. ^ Gal J (1982). "Amphetamines in Nasal Inhalers". Journal of Toxicology: Clinical Toxicology. 19 (5): 517–518. doi:10.3109/15563658208992508. ISSN 0731-3810.
  68. ^ Halle AB, Kessler R, Alvarez M (June 1985). "Drug abuse with Vicks nasal inhaler". South Med J. 78 (6): 761–2. doi:10.1097/00007611-198506000-00043. PMID 4002016.
  69. ^ Ferrando RL, McCorvey E, Simon WA, Stewart DM (March 1988). "Bizarre behavior following the ingestion of levo-desoxyephedrine". Drug Intell Clin Pharm. 22 (3): 214–217. doi:10.1177/106002808802200308. PMID 3366062.
  70. ^ Arnold LE, Huestis RD, Smeltzer DJ, Scheib J, Wemmer D, Colner G (March 1976). "Levoamphetamine vs dextroamphetamine in minimal brain dysfunction. Replication, time response, and differential effect by diagnostic group and family rating". Arch Gen Psychiatry. 33 (3): 292–301. doi:10.1001/archpsyc.1976.01770030012002. PMID 769721.
  71. ^ Parkes JD, Fenton GW (December 1973). "Levo(-) amphetamine and dextro(+) amphetamine in the treatment of narcolepsy". J Neurol Neurosurg Psychiatry. 36 (6): 1076–81. doi:10.1136/jnnp.36.6.1076. PMC 1083612. PMID 4359162.
  72. ^ Arnold LE, Kirilcuk V, Corson SA, Corson EO (February 1973). "Levoamphetamine and dextroamphetamine: differential effect on aggression and hyperkinesis in children and dogs". Am J Psychiatry. 130 (2): 165–70. doi:10.1176/ajp.130.2.165. PMID 4568123.
  73. ^ Gillin JC, van Kammen DP, Graves J, Murphy D (October 1975). "Differential effects of D- and L-amphetamine on the sleep of depressed patients". Life Sci. 17 (8): 1223–1240. doi:10.1016/0024-3205(75)90132-0. PMID 172755.
  74. ^ Hartmann E, Cravens J (November 1976). "Sleep: effects of d- and l-amphetamine in man and in rat". Psychopharmacology (Berl). 50 (2): 171–175. doi:10.1007/BF00430488. PMID 826958.
  75. ^ Janowsky DS, Davis JM (March 1976). "Methylphenidate, dextroamphetamine, and levamfetamine. Effects on schizophrenic symptoms". Arch Gen Psychiatry. 33 (3): 304–308. doi:10.1001/archpsyc.1976.01770030024003. PMID 769722.
  76. ^ Hartmann E, Orzack MH, Branconnier R (July 1977). "Sleep deprivation deficits and their reversal by d- and l-amphetamine". Psychopharmacology (Berl). 53 (2): 185–189. doi:10.1007/BF00426490. PMID 408844.
  77. ^ Caine ED, Ludlow CL, Polinsky RJ, Ebert MH (March 1984). "Provocative drug testing in Tourette's syndrome: d- and l-amphetamine and haloperidol". J Am Acad Child Psychiatry. 23 (2): 147–152. doi:10.1097/00004583-198403000-00005. PMID 6585416.
  78. ^ Parkes JD, Tarsy D, Marsden CD, Bovill KT, Phipps JA, Rose P, et al. (March 1975). "Amphetamines in the treatment of Parkinson's disease". J Neurol Neurosurg Psychiatry. 38 (3): 232–7. doi:10.1136/jnnp.38.3.232. PMC 491901. PMID 1097600.
  79. ^ Patti F (November 2012). "Treatment of cognitive impairment in patients with multiple sclerosis". Expert Opin Investig Drugs. 21 (11): 1679–1699. doi:10.1517/13543784.2012.716036. PMID 22876911.
  80. ^ Lovera J, Kovner B (October 2012). "Cognitive impairment in multiple sclerosis". Curr Neurol Neurosci Rep. 12 (5): 618–627. doi:10.1007/s11910-012-0294-3. PMC 4581520. PMID 22791241.
  81. ^ Roy S, Benedict RH, Drake AS, Weinstock-Guttman B (March 2016). "Impact of Pharmacotherapy on Cognitive Dysfunction in Patients with Multiple Sclerosis". CNS Drugs. 30 (3): 209–225. doi:10.1007/s40263-016-0319-6. PMID 26884145.
  82. ^ Morrow SA, Kaushik T, Zarevics P, Erlanger D, Bear MF, Munschauer FE, et al. (July 2009). "The effects of L-amphetamine sulfate on cognition in MS patients: results of a randomized controlled trial". J Neurol. 256 (7): 1095–102. doi:10.1007/s00415-009-5074-x. PMID 19263186.
  83. ^ Benedict RH, Munschauer F, Zarevics P, Erlanger D, Rowe V, Feaster T, et al. (June 2008). "Effects of l-amphetamine sulfate on cognitive function in multiple sclerosis patients". J Neurol. 255 (6): 848–852. doi:10.1007/s00415-008-0760-7. PMID 18481035.
  84. ^ Sumowski JF, Chiaravalloti N, Erlanger D, Kaushik T, Benedict RH, DeLuca J (September 2011). "L-amphetamine improves memory in MS patients with objective memory impairment". Mult Scler. 17 (9): 1141–1145. doi:10.1177/1352458511404585. PMID 21561956.
  85. ^ "Levafetamine". AdisInsight. 2 October 2021. Retrieved 28 October 2024.
  86. ^ a b c Mahmood I (August 1997). "Clinical pharmacokinetics and pharmacodynamics of selegiline. An update". Clin Pharmacokinet. 33 (2): 91–102. doi:10.2165/00003088-199733020-00002. PMID 9260033.
  87. ^ a b c Miklya I (November 2016). "The significance of selegiline/(-)-deprenyl after 50 years in research and therapy (1965-2015)". Mol Psychiatry. 21 (11): 1499–1503. doi:10.1038/mp.2016.127. PMID 27480491.
  88. ^ a b Tábi T, Vécsei L, Youdim MB, Riederer P, Szökő É (May 2020). "Selegiline: a molecule with innovative potential". J Neural Transm (Vienna). 127 (5): 831–842. doi:10.1007/s00702-019-02082-0. PMC 7242272. PMID 31562557.
  89. ^ Poston KL, Waters C (October 2007). "Zydis selegiline in the management of Parkinson's disease". Expert Opin Pharmacother. 8 (15): 2615–2624. doi:10.1517/14656566.8.15.2615. PMID 17931095.
  90. ^ Chrisp P, Mammen GJ, Sorkin EM (May 1991). "Selegiline: A Review of its Pharmacology, Symptomatic Benefits and Protective Potential in Parkinson's Disease". Drugs Aging. 1 (3): 228–248. doi:10.2165/00002512-199101030-00006. PMID 1794016.
  91. ^ a b c Gerlach M, Reichmann H, Riederer P (2012). "A critical review of evidence for preclinical differences between rasagiline and selegiline". Basal Ganglia. 2 (4): S9–S15. doi:10.1016/j.baga.2012.04.032.
  92. ^ Yasar S, Goldberg JP, Goldberg SR (1 January 1996). "Are metabolites of l-deprenyl (Selegiline) useful or harmful? Indications from preclinical research". Deprenyl — Past and Future. Journal of Neural Transmission. Supplementum. Vol. 48. pp. 61–73. doi:10.1007/978-3-7091-7494-4_6. ISBN 978-3-211-82891-5. PMID 8988462.
  93. ^ Finberg JP (April 2019). "Inhibitors of MAO-B and COMT: their effects on brain dopamine levels and uses in Parkinson's disease". Journal of Neural Transmission. 126 (4): 433–448. doi:10.1007/s00702-018-1952-7. PMID 30386930.
  94. ^ Simpson LL (1978). "Evidence that deprenyl, A type B monoamine oxidase inhibitor, is an indirectly acting sympathomimetic amine". Biochem Pharmacol. 27 (11): 1591–1595. doi:10.1016/0006-2952(78)90490-2. PMID 697901.
  95. ^ Abassi ZA, Binah O, Youdim MB (October 2004). "Cardiovascular activity of rasagiline, a selective and potent inhibitor of mitochondrial monoamine oxidase B: comparison with selegiline". Br J Pharmacol. 143 (3): 371–378. doi:10.1038/sj.bjp.0705962. PMC 1575354. PMID 15339864.
  96. ^ Dezsi L, Vecsei L (2017). "Monoamine Oxidase B Inhibitors in Parkinson's Disease". CNS Neurol Disord Drug Targets. 16 (4): 425–439. doi:10.2174/1871527316666170124165222. PMID 28124620.
  97. ^ Musshoff F (February 2000). "Illegal or legitimate use? Precursor compounds to amphetamine and methamphetamine". Drug Metab Rev. 32 (1): 15–44. doi:10.1081/dmr-100100562. PMID 10711406.
  98. ^ Cody JT (May 2002). "Precursor medications as a source of methamphetamine and/or amphetamine positive drug testing results". J Occup Environ Med. 44 (5): 435–450. doi:10.1097/00043764-200205000-00012. PMID 12024689.
[edit]
Retrieved from "https://wiki.riteme.site/w/index.php?title=Levoamphetamine&oldid=1257683493"