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Levomethamphetamine

(Redirected from Levmetamfetamine)

Levomethamphetamine,[note 1] sold under the brand name Vicks Vapor Inhaler among others, is a sympathomimetic, decongestant, and stimulant medication which is used to treat nasal congestion.[1] It is available over-the-counter at low doses as a decongestant in the United States and is taken by inhalation for this use.[1]

Levomethamphetamine
INN: Levmetamfetamine
Clinical data
Trade namesVicks Vapor Inhaler[1]
Other namesLevmetamfetamine; L-Methamphetamine; R-(-)-Methamphetamine; Levodesoxyephedrine; L-Desoxyephedrine
Routes of
administration		Medical: Inhalation (nasal)
Recreational: Oral, intravenous, insufflation, inhalation, suppository
Legal status
Legal status
Pharmacokinetic data
BioavailabilityOral: ~100%[1][3]
MetabolismLiver
MetabolitesLevoamphetamine[1][4][3]
Elimination half-life10–15 hours[1][4][3]
ExcretionUrine (41–49% unchanged, 2–3% as levoamphetamine)[1][4][3]
Identifiers
  • (R)-N-methyl-1-phenyl-propan-2-amine
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
CompTox Dashboard (EPA)
ECHA InfoCard100.046.974 Edit this at Wikidata
Chemical and physical data
FormulaC10H15N
Molar mass149.237 g·mol−1
3D model (JSmol)
  • N([C@@H](Cc1ccccc1)C)C
  • InChI=1S/C10H15N/c1-9(11-2)8-10-6-4-3-5-7-10/h3-7,9,11H,8H2,1-2H3/t9-/m1/s1 checkY
  • Key:MYWUZJCMWCOHBA-SECBINFHSA-N checkY
 ☒NcheckY (what is this?)  (verify)

Levomethamphetamine act as a selective releasing agent of norepinephrine.[5][6][4] It also induces the release of dopamine to a far lesser extent.[5][7][4] Levomethamphetamine is an amphetamine and is the levorotatory enantiomer of the better-known methamphetamine.[1] The effects of levomethamphetamine are distinct from those of racemic methamphetamine and dextromethamphetamine and it does not have the same misuse potential as these substances.[1][8][9][4][10]

Medical uses

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Nasal decongestion

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Levomethamphetamine is used as a nasal decongestant.[1]

Available forms

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Levomethamphetamine is available in the form of decongestant inhalers containing 50 mg total levomethamphetamine per inhaler and delivering between 0.04 and 0.15 mg of the drug per inhalation.[1] Inhalers with a total of 113 mg levomethamphetamine were previously marketed in the United States, but the total amount was reduced to 50 mg starting in 2009.[1]

Side effects

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When the nasal decongestant is taken in excess, levomethamphetamine has potential side effects. These would be similar to those of other decongestants.

Pharmacology

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Pharmacodynamics

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Levomethamphetamine acts as a selective norepinephrine releasing agent.[6][5][7][4] Whereas dextromethamphetamine is a relatively balanced releaser of dopamine and norepinephrine, levomethamphetamine is about 15-fold less potent in inducing dopamine release relative to norepinephrine.[5][7][4] Accordingly, levomethamphetamine and the related compound levoamphetamine are 10 times less potent at stimulating locomotor activity (a measure of psychostimulant effect) than dextromethamphetamine and dextroamphetamine in rodents.[11][12]

Monoamine release of levomethamphetamine and related substances (EC50Tooltip Half maximal effective concentration, nM)[5][13]
Compound 5-HTTooltip Serotonin NETooltip Norepinephrine DATooltip Dopamine Type Class Ref
Amphetamine ND ND ND NDRA Amphetamine ND
  D-Amphetamine 698–1765 6.6–7.2 5.8–24.8 NDRA Amphetamine [6][14]
  L-Amphetamine ND ND ND NRA Amphetamine ND
Ephedrine ND ND ND NDRA Cathinol ND
  D-Ephedrine >10000 43.1–72.4 236–1350 NDRA Cathinol [6]
  L-Ephedrine >10000 218 2104 NRA Cathinol [6][15]
Methamphetamine ND ND ND NDRA Amphetamine ND
  D-Methamphetamine 736–1291.7 12.3–13.8 8.5–24.5 NDRA Amphetamine [6][16]
  L-Methamphetamine 4640 28.5 416 NRA Amphetamine [6]
Pseudoephedrine ND ND ND NDRA Cathinol ND
  D-Pseudoephedrine >10000 4092 9125 NDRA Cathinol [15]
  L-Pseudoephedrine >10000 224 1988 NRA Cathinol [15]
Note: The smaller the value, the more strongly the substance releases the neurotransmitter.

The effects of levomethamphetamine are qualitatively distinct relative to those of racemic methamphetamine and dextromethamphetamine and it does not possess the same potential for euphoria or addiction that these drugs possesses.[1][8][9][4][10] In clinical studies, levomethamphetamine at oral doses of 1 to 10 mg has been found not to affect subjective drug responses, heart rate, blood pressure, core temperature, electrocardiography, respiration rate, oxygen saturation, or other clinical parameters.[1][3] As such, doses of levomethamphetamine of less than or equal to 10 mg have no significant physiological or subjective effects.[1][3] However, higher doses of levomethamphetamine, for instance 0.25 to 0.5 mg/kg (mean doses of ~18–37 mg) intravenously, have been reported to produce significant pharmacological effects, including increased heart rate and blood pressure, increased respiration rate, and subjective effects like intoxication and drug liking.[1][4] On the other hand, in contrast to dextromethamphetamine, levomethamphetamine also produces subjective "bad" or aversive drug effects.[7][4] Among the physiological effects of levomethamphetamine is vasoconstriction, which makes it useful for nasal decongestion.[17]

As with levomethamphetamine, 20 to 60 mg oral doses of the related drug levoamphetamine have been reported to produce significant effects, for instance on wakefulness and mood.[18][19][20][21]

In addition to its norepinephrine-releasing activity, levomethamphetamine is also an agonist of the trace amine-associated receptor 1 (TAAR1).[22][23][24]

Pharmacokinetics

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The bioavailability of levomethamphetamine is approximately 100%.[1][3] The peak levels of levomethamphetamine range from 3.3 to 31.4 ng/mL with single oral doses of 1 to 10 mg and from 65.4 to 125.9 ng/mL with single intravenous doses of 0.25 to 0.5 mg/kg.[1][4][25] The area-under-the-curve (AUC) levels of levomethamphetamine range from 73.0 to 694.7 ng⋅h/mL with single oral doses of 1 to 10 mg and from 1190.7 to 2368.1 mg/kg with single intravenous doses of 0.25 to 0.5 mg/kg.[1][4][25]

The volume of distribution of levomethamphetamine is 288.5 to 315.5 L or 4.15 to 4.17 L/kg.[1][4][3]

The mean elimination half-life of levomethamphetamine ranges between 10.2 and 15.0 hours.[1][4] For comparison, the elimination half-life of dextromethamphetamine was around around 10.2 to 10.7 hours in the same studies.[1][4] The clearance of levomethamphetamine is 15.5 to 19.1 L/h or 0.221 L/h⋅kg.[1][4][3]

Levomethamphetamine is excreted in urine 40.8 to 49.0% as unchanged levomethamphetamine and 2.1 to 3.3% as levoamphetamine.[1][4][3]

Chemistry

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Detection in body fluids

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Levomethamphetamine can register on urine drug tests as either methamphetamine, amphetamine, or both, depending on the subject's metabolism and dosage. Levomethamphetamine metabolizes completely into levoamphetamine after a period of time.[26]

Society and culture

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Recreational use

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As of 2006, there were no studies demonstrating "drug liking" scores of oral levomethamphetamine that are similar to racemic methamphetamine or dextromethamphetamine in either recreational users or medicinal users.[4] In any case, misuse of levomethamphetamine at high doses has been reported.[27][28][29][30]

In recent years, tighter controls in Mexico on certain methamphetamine precursors like ephedrine and pseudoephedrine has led to a greater percentage of illicit methamphetamine from Mexican drug cartels consisting of a higher ratio of levomethamphetamine to dextromethamphetamine within batches of racemic methamphetamine.[31] However, in recent years, cartels have used chiral separation to produce relatively pure dextromethamphetamine from the racemic substance.

Other drugs

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Selegiline

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Main article: Selegiline

Levomethamphetamine is an active metabolite of the antiparkinsonian and antidepressant medication selegiline. Selegiline, a selective monoamine oxidase B (MAOB) inhibitor at low doses,[note 2] is also metabolized into levomethamphetamine and levoamphetamine.[32][33] This has caused users to test positive for amphetamines.[34][35] With a 10 mg oral dose of selegiline, about 2 to 6 mg levomethamphetamine and 1 to 3 mg levoamphetamine is excreted in urine.[36][37][38] Selegiline itself has neuroprotective and neurorestorative effects, but concern over the resulting levomethamphetamine's side effects and potential neurotoxicity led to development of alternative MAOB inhibitors, such as rasagiline, that do not produce toxic metabolites.[39][40]

Notes

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  1. ^ Other names include levmetamfetamine (INNTooltip International Nonproprietary Name), L-methamphetamine, R-(-)-methamphetamine, levodesoxyephedrine, and L-desoxyephedrine.
  2. ^ It is a selective MAOB inhibitor at normal clinical doses. MAOB is an enzyme that metabolizes dopamine, the neurotransmitter deficient in Parkinson's disease.

References

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  1. ^ a b c d e f g h i j k l m n o p q r s t u v w x 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.
  2. ^ Anvisa (31 March 2023). "RDC Nº 784 - Listas de Substâncias Entorpecentes, Psicotrópicas, Precursoras e Outras sob Controle Especial" [Collegiate Board Resolution No. 784 - Lists of Narcotic, Psychotropic, Precursor, and Other Substances under Special Control] (in Brazilian Portuguese). Diário Oficial da União (published 4 April 2023). Archived from the original on 3 August 2023. Retrieved 16 August 2023.
  3. ^ a b c d e f g h i j Li L, Lopez JC, Galloway GP, Baggott MJ, Everhart T, Mendelson J (August 2010). "Estimating the intake of abused methamphetamines using experimenter-administered deuterium labeled R-methamphetamine: selection of the R-methamphetamine dose". Ther Drug Monit. 32 (4): 504–7. doi:10.1097/FTD.0b013e3181db82f2. PMC 3040572. PMID 20592647.
  4. ^ a b c d e f g h i j k l m n o p q r s Mendelson J, Uemura N, Harris D, Nath RP, Fernandez E, Jacob P, et al. (October 2006). "Human pharmacology of the methamphetamine stereoisomers". Clin Pharmacol Ther. 80 (4): 403–420. doi:10.1016/j.clpt.2006.06.013. PMID 17015058. The stereoisomers of methamphetamine produce markedly different dopamine, norepinephrine, and serotonin responses in various brain regions in rats.41,42 d-Methamphetamine (2 mg/kg) is more potent in releasing caudate dopamine than l-methamphetamine (12 and 18 mg/kg). By use of in vitro uptake and release assays, d-methamphetamine (50% effective concentration [EC50], 24.5 ± 2.1 nmol/L) was 17 times more potent in releasing dopamine than l-methamphetamine (EC50, 416 ± 20 nmol/L) and significantly more potent in blocking dopamine uptake (inhibition constant [Ki ], 114 ± 11 nm versus 4840 ± 178 nm).12,13
  5. ^ a b c d e 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.
  6. ^ a b c d e f g 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.
  7. ^ a b c d Kohut SJ, Jacobs DS, Rothman RB, Partilla JS, Bergman J, Blough BE (December 2017). "Cocaine-like discriminative stimulus effects of "norepinephrine-preferring" monoamine releasers: time course and interaction studies in rhesus monkeys". Psychopharmacology (Berl). 234 (23–24): 3455–3465. doi:10.1007/s00213-017-4731-5. PMC 5747253. PMID 28889212. In the present experiments, two monoamine releasers, l-MA and PAL-329, were shown to produce cocaine-like discriminative-stimulus effects in monkeys, suggesting that they meet the above criteria. One of these compounds, l-MA, also has been shown to serve as a positive reinforcer in rodents (Yokel and Pickens 1973) and monkeys (Winger et al 1994), further confirming the overlap with behavioral effects of cocaine. Both compounds also exhibit an approximately 15-fold greater potency in releasing NE than DA, which may be therapeutically advantageous. For example, the subjective effects of l-MA in human studies are similar in some respects to those of d-MA. However, the subjective effects of the two isomers also differ in potentially important ways. While both l-MA and d-MA produce subjective ratings of "drug liking" and "good effects" in experienced stimulant users, only lMA produces concomitant ratings of bad or aversive drug effects (Mendelson et al 2006), a factor which may limit its abuse liability.
  8. ^ a b Pauly RC, Bhimani RV, Li JX, Blough BE, Landavazo A, Park J (March 2023). "Distinct Effects of Methamphetamine Isomers on Limbic Norepinephrine and Dopamine Transmission in the Rat Brain". ACS Chemical Neuroscience: acschemneuro.2c00689. doi:10.1021/acschemneuro.2c00689. PMID 36976755. S2CID 257772503.
  9. ^ a b Melega WP, Cho AK, Schmitz D, Kuczenski R, Segal DS (February 1999). "l-methamphetamine pharmacokinetics and pharmacodynamics for assessment of in vivo deprenyl-derived l-methamphetamine". The Journal of Pharmacology and Experimental Therapeutics. 288 (2): 752–758. PMID 9918585.
  10. ^ 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". The Journal of Neuroscience. 15 (2): 1308–1317. doi:10.1523/jneurosci.15-02-01308.1995. PMC 6577819. PMID 7869099.
  11. ^ 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. The D,L-racemic mixture of deprenyl was developed in Hungary by Knoll in 1964 as a novel MAO-inhibitor antidepressant [9]. [...] More importantly, the D-isomer is metabolised to D-amphetamine and D-methamphetamine [11], which have ten times the amphetamine potency of the corresponding L-isomers [12].
  12. ^ 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.
  13. ^ 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.
  14. ^ 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.
  15. ^ 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.
  16. ^ 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.
  17. ^ Pray SW (19 February 2010). "Nonprescription Products to Avoid With Hypertension". uspharmacist.com. Archived from the original on 30 October 2014. Retrieved 17 October 2014. Topical Nasal Decongestants: Most topical nasal decongestants also carry the warning against unsupervised use with hypertension. This includes oxymetazoline (e.g., Afrin), phenylephrine (e.g., Neo-Synephrine), naphazoline (e.g., Privine), and l-desoxyephedrine/levomethamphetamine. When hypertensive patients request a nasal decongestant, the pharmacist can recommend several alternatives. Propylhexedrine (e.g., Benzedrex Inhaler) is not required to carry a warning against unsupervised use with hypertension and may be effective. Another option is the nasal strip (e.g., Breathe Right). When properly applied, the strip can open the nostrils slightly, and perhaps sufficiently to allow the patient to breathe without use of a pharmacologically active ingredient.
  18. ^ 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. A comparison of dextroamphetamine and levoamphetamine revealed that the dextrorotatory isomer was the more potent in elevating mood in normal subjects, being at least twice as potent as the levo form.35 [...] Narcolepsy was one of the first conditions to be treated successfully with amphetamine3 and remains one of the few (some would say the only) clinical indications for its use. While the required oral dose of dextroamphetamine (Dexedrine®) ranges from 5 to 120 mg/day, most patients respond to 10 mg two to four times daily. [...] The closely related compound methylphenidate (Ritalin®), 20 mg two to four times daily, has been shown to be as effective as dextroamphetamine but with less likelihood of causing side effects.61 The same is true of levoamphetamine.62 [...] Nevertheless, as amphetamine has an action on dopaminergic pathways it was considered worthwhile to examine the effects of amphetamine under controlled conditions.95 Twenty patients, all on other anti-Parkinsonian drugs, were studied. There was some subjective improvement in a proportion (less than half) of the patients when they received either dextroamphetamine or levoamphetamine, but there was little objective improvement. The authors remarked that amphetamine was unlikely to have worked anyway in Parkinson's disease as it acts mainly by releasing dopamine and noradrenaline from presynaptic neurons; as the underlying pathology involves a reduction of presynaptic dopamine, there would be insufficient dopamine for amphetamine to release.
  19. ^ 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.
  20. ^ 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.
  21. ^ 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.
  22. ^ "Levmetamfetamine". PubChem. National Center for Biotechnology Information, U.S. National Library of Medicine. Archived from the original on 18 October 2014. Retrieved 17 October 2014.
  23. ^ 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.
  24. ^ 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.
  25. ^ a b Li L, Everhart T, Jacob Iii P, Jones R, Mendelson J (February 2010). "Stereoselectivity in the human metabolism of methamphetamine". Br J Clin Pharmacol. 69 (2): 187–192. doi:10.1111/j.1365-2125.2009.03576.x. PMC 2824480. PMID 20233182.
  26. ^ DeGeorge M, Weber J (30 November 2012). "Methamphetamine Urine Toxicology: An In-depth Review". Practical Pain Management. Vertical Health LLC. Archived from the original on 13 February 2016. Retrieved 21 February 2016.
  27. ^ 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. The 64-inhalation condition produced a small (change score of ~6) increase in "Good Drug Effect" suggesting a low potential for abuse even though occurrences of inhaler abuse is reported in the literature [1,18,19]. Larger doses of intravenous lmethamphetamine are psychoactive and may have some abuse potential in methamphetamine users [16].
  28. ^ Gal J (1982). "Amphetamines in Nasal Inhalers". Journal of Toxicology: Clinical Toxicology. 19 (5): 517–518. doi:10.3109/15563658208992508. ISSN 0731-3810.
  29. ^ 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.
  30. ^ 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.
  31. ^ Cunningham JK, Maxwell JC, Campollo O, Liu LM, Lattyak WJ, Callaghan RC (April 2013). "Mexico's precursor chemical controls: emergence of less potent types of methamphetamine in the United States". Drug Alcohol Depend. 129 (1–2): 125–36. doi:10.1016/j.drugalcdep.2012.10.001. PMID 23127541.
  32. ^ Kalász H, Magyar K, Szőke É, Adeghate E, Adem A, Hasan MY, et al. (1 January 2014). "Metabolism of selegiline [(-)-deprenyl)]". Current Medicinal Chemistry. 21 (13): 1522–1530. doi:10.2174/0929867321666131218094352. PMID 24350849.
  33. ^ Magyar K (1 January 2011). "The pharmacology of selegiline". International Review of Neurobiology. 100: 65–84. doi:10.1016/B978-0-12-386467-3.00004-2. ISBN 9780123864673. PMID 21971003.
  34. ^ Cody JD (December 1993). "Metabolic Precursors to Amphetamine and Methamphetamine". Forensic Science Review. 5 (2): 109–127. PMID 26270078.
  35. ^ Cody JT (May 2002). "Precursor medications as a source of methamphetamine and/or amphetamine positive drug testing results". Journal of Occupational and Environmental Medicine. 44 (5): 435–450. doi:10.1097/00043764-200205000-00012. PMID 12024689. S2CID 44614179.
  36. ^ Poston KL, Waters C (October 2007). "Zydis selegiline in the management of Parkinson's disease". Expert Opin Pharmacother. 8 (15): 2615–24. doi:10.1517/14656566.8.15.2615. PMID 17931095.
  37. ^ 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.
  38. ^ 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): 228–48. doi:10.2165/00002512-199101030-00006. PMID 1794016.
  39. ^ Tabakman R, Lecht S, Lazarovici P (January 2004). "Neuroprotection by monoamine oxidase B inhibitors: a therapeutic strategy for Parkinson's disease?". BioEssays. 26 (1): 80–90. doi:10.1002/bies.10378. PMID 14696044.
  40. ^ Kong P, Zhang B, Lei P, Kong X, Zhang S, Li D, et al. (1 January 2015). "Neuroprotection of MAO-B inhibitor and dopamine agonist in Parkinson disease". International Journal of Clinical and Experimental Medicine. 8 (1): 431–439. PMC 4358469. PMID 25785014.
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