Talk:Levoamphetamine

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Summary sheet: Levoamphetamine

Levoamphetamine
Chemical Nomenclature
Common names	Levoamphetamine
Substitutive name	l-Amphetamine
Systematic name	(2R)-1-Phenylpropan-2-amine
Class Membership
Psychoactive class	Stimulant
Chemical class	Phenethylamine
Routes of Administration
WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section. ⇣ Oral Dosage Bioavailability 20-25-75%+ Threshold 2.5 mg Light 5 - 10 mg Common 10 - 25 mg Strong 25 - 50 mg Heavy 50 mg + Duration Total 6 - 8 hours Onset 30 - 45 minutes Come up 30 - 135 minutes Peak 2.5 - 4 hours Offset 2 - 3 hours After effects 3 - 6 hours ⇣ Insufflated Dosage Bioavailability 75% Threshold 4 mg Light 6 - 15 mg Common 15 - 30 mg Strong 30 - 50 mg Heavy 50 mg + Duration Total 3 - 6 hours Onset 1 - 5 minutes Come up 30 - 90 minutes Peak 1 - 2 hours Offset 1.5 - 3 hours After effects 2 - 4 hours ⇣ Intravenous Dosage Bioavailability 100% Threshold 4 mg Light 6 - 15 mg Common 15 - 30 mg Strong 30 - 50 mg Heavy 50 mg + Duration Total 3 - 6 hours Onset 2 - 10 seconds Come up 2 - 10 seconds Peak 2 - 4 hours Offset 1 - 2 hours After effects 1.5 - 4 hours DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Levoamphetamine (also known as Levamphetamine, l-Amphetamine, or by brand names including Adderall) is a stimulant substance and the left-handed enantiomer of amphetamine.

Levoamphetamine is the less potent isomer of the two, but the effects are also slightly different in character. The small difference in affinity affects the mechanism resulting in a more physically focused stimulation rather than mental.

Dangerous interactions

Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).

Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

• Alcohol - Drinking alcohol on stimulants is considered risky because it reduces the sedative effects of the alcohol that the body uses to gauge drunkenness. This often leads to excessive drinking with greatly reduced inhibitions, increasing the risk of liver damage and increased dehydration. The effects of stimulants will also allow one to drink past a point where they might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel the alcohol and the stimulant less.
• GHB/GBL - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the depressant effects of the GHB/GBL may over come the user and cause respiratory arrest.
• Benzodiazepines - These substances can strongly mitigate the comedown of Stimulants and allow higher doses of them, which is a dangerous combination. And through the habit-forming properties, these substances should be consumed with extreme caution.
• Opioids - Opioids combined with amphetamines have been found to potentially synergize unpredictably, increasing the chance of overdose. Stimulants also increase respiration rate allowing a higher dose of opioids. If the stimulant wears off first, then the opiate may overcome the patient and cause respiratory arrest.
• Cocaine - The rewarding effects of cocaine are mediated by DAT inhibition, and an increase of exocytosis of dopamine through the cell membrane. Amphetamine reverses the direction of DAT and the direction vesicular transports within the cell by a pH mediated mechanism of displacement, thus excludes the regular mechanism of dopamine release through means of exocytosis because the effects Na+/K+ ATPase are inhibited. You will find cardiac effects with the combination of cocaine and amphetamine due to a SERT mediated mechanism from the subsequent activation of 5-HT2B, which is an effect of serotonin-related valvulopathy. Amphetamines generally cause hypertension in models of abuse, and this combination can increase the chances of syncope due to turbulent blood flow during valve operation. The rewarding mechanisms of cocaine are reversed by administration of amphetamine.
• Cannabis - Stimulants increase anxiety levels and the risk of thought loops and paranoia, which can lead to negative experiences.
• Caffeine - This combination of stimulants is generally considered unnecessary and may increase strain on the heart, as well as potentially causing anxiety and physical discomfort.
• Tramadol - Tramadol and stimulants both increase the risk of seizures.
• DXM - Both substances raise heart rate; in extreme cases, panic attacks caused by these substances have led to more serious heart issues.
• Ketamine - Combining amphetamine and ketamine may result in psychosis that resembles schizophrenia, but not worse than the psychosis produced by either substance alone, but this is debatable. This is due to amphetamines ability to attenuated the disruption of working memory caused by ketamine. Amphetamine alone may result in grandiosity, paranoia, or somatic delusions with little to no effect on negative symptoms. Ketamine, however, will result in thought disorders, disruption of executive functioning, and delusions due to a modification of conception. These mechanisms are due to an increase of dopaminergic activity in the mesolimbic pathway caused by amphetamine due to its pharmacology effecting dopamine, and due to a disruption of dopaminergic functioning in the mesocortical pathways via NMDA antagonism effects of ketamine. Combining the two, you may expect mainly thought disorder along with positive symptoms.
• PCP - Increases risk of tachycardia, hypertension, and manic states.
• Methoxetamine - Increases risk of tachycardia, hypertension, and manic states.
• Gabapentinoids - Gabapentinoids like Pregabalin or Gabapentin can mitigate the comedown of Stimulants, but through the very fast tolerance development the effects will become less after a few days
• Psychedelics (e.g. LSD, mescaline, psilocybin) - Increases risk of anxiety, paranoia, and thought loops.
  • 25x-NBOMe - Amphetamines and NBOMes both provide considerable stimulation that when combined they can result in tachycardia, hypertension, vasoconstriction and, in extreme cases, heart failure. The anxiogenic and focusing effects of stimulants are also not good in combination with psychedelics, as they can lead to unpleasant thought loops. NBOMes are known to cause seizures, and stimulants can increase this risk.
  • 2C-T-x - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
  • 5-MeO-xxT - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
  • DOx
• aMT - aMT has MAOI properties which may interact unfavorably with amphetamines.
• MAOIs - MAO-B inhibitors can increase the potency and duration of phenethylamines unpredictably. MAO-A inhibitors with amphetamine can lead to hypertensive crises.
• Acetazolamide - Administration may increase serum concentration of amphetamine.
• Ascorbic acid - Lowers urinary pH; may enhance amphetamine excretion.
  • Furazolidone - Amphetamines may induce a hypertensive response in patients taking furazolidone.
• Guanethidine - Amphetamine inhibits the antihypertensive response to guanethidine.
• Haloperidol - Limited evidence indicates that haloperidol may inhibit the effects of amphetamine but the clinical importance of this interaction is not established.
• Lithium carbonate - Isolated case reports indicate that lithium may inhibit the effects of amphetamine.
• Norepinephrine - Amphetamine abuse may enhance the pressor response to norepinephrine.
• Phenothiazines - Amphetamine may inhibit the antipsychotic effect of phenothiazines, and phenothiazines may inhibit the anorectic effect of amphetamines.
• Sodium bicarbonate - Large doses of sodium bicarbonate inhibit the elimination of amphetamine, thus increasing the amphetamine effect.
• TCAs - Theoretically increases the effect of amphetamine, but clinical evidence is lacking.

Legal status

Internationally, amphetamine (and its isomers dextroamphetamine and levoamphetamine) are Schedule II controlled substances under the United Nations 1971 Convention on Psychotropic Substances.

• Australia: Levoamphetamine is a Schedule 8 controlled substance.
• Austria: Levoamphetamine is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).
• Germany: Levoamphetamine is controlled under Anlage II BtMG (Narcotics Act, Schedule II), in contrast to dextroamphetamine and racemic amphetamine which fall under Anlage III BtMG (Narcotics Act, Schedule III).
• The Netherlands: Levoamphetamine is a List I controlled substance.
• South Korea: Levoamphetamine is prohibited even for medical use in South Korea in compliance with the United Nations Convention on Psychotropic Substances.
• United Kingdom: Amphetamine is a Class B drug in the United Kingdom, without any clarification about isomers.
• United States: Amphetamine is a Schedule IIN controlled substance in the United States, citing several prescription drugs as some of which contain levo amphetamine.

See also

• Responsible use
• Stimulant
• Amphetamine

External links

• Levoamphetamine (Wikipedia)