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Stimulant

Methamphetamine

Also called Meth, Crystal, Desoxyn, Speed, Ma, Ice, Glass, Shard, Tina, T, Tweak, Crank, Shabu, Yaba

Original Wikipedia articleen.wikipedia.org/wiki/Methamphetamine revision used (24 October 2026)

Why a "revision used" link? Anyone can edit Wikipedia at any time, so the article you open today may not say what it said when we read it. This link opens the exact version we read on 24 October 2026, frozen as it was. It is the only way to check that every quote on this page matches its source word for word. Newer versions may correct or change things. When we re-check this page against a newer version, the edit log records it. How we cite

Common dose · Oral10–25 mg PW
Onset15–45 minutes PW
Total8–12 hours Up to 24h for irregular users. PW
After-effects12–24 hours PW

Dosage

When sources disagree, both rows are shown as published. Nothing is averaged or merged.

Oral

SourceThresholdLightCommonStrongHeavy
PsychonautWiki< 5 mg PW5–10 mg PW10–25 mg PW25–50 mg PW50 mg+ PW
TripSit–5–10 mg TS10–30 mg TS20–40 mg TS40–100 mg TS

Bioavailability: ~70%[8] PW

Rectal

SourceThresholdLightCommonStrongHeavy
PsychonautWiki< 5 mg PW5–10 mg PW10–30 mg PW30–40 mg PW40 mg+ PW

Bioavailability: ~99%[18] PW

Smoked

SourceThresholdLightCommonStrongHeavy
PsychonautWiki< 5 mg PW5–10 mg PW10–20 mg PW20–60 mg PW60 mg+ PW
TripSit–5–10 mg TS10–20 mg TS30–60 mg TS50 mg+ TS

Bioavailability: >90% PW

Insufflated

SourceThresholdLightCommonStrongHeavy
PsychonautWiki< 5 mg PW5–10 mg PW10–30 mg PW30–60 mg PW60 mg+ PW
TripSit–5–10 mg TS10–30 mg TS30–50 mg TS50 mg+ TS

Bioavailability: >90% PW

Intravenous

SourceThresholdLightCommonStrongHeavy
PsychonautWiki< 5 mg PW5–10 mg PW10–30 mg PW30–40 mg PW40 mg+ PW
TripSit–5–10 mg TS10–20 mg TS20–40 mg TS40 mg+ TS

Bioavailability: ~100%[8] PW

TripSit dose text

TripSit's factsheet also states its doses as text.

Oral Light: 5-10mg Common: 10-30mg Strong: 20-40mg Heavy: 40-100mg | Insufflated Light: 5-10mg Common: 10-30mg Strong: 30-50mg Heavy: 50mg+ | Smoked Light: 5-10mg Common: 10-20mg Strong: 30-60mg Heavy: 50mg+ | IV Light: 5-10mg Common: 10-20mg Strong: 20-40mg Heavy: 40mg+ TS

What dose are you on? (self-reported, unverified)
Read this first. These numbers come from anonymous visitors typing in a box. Nobody checks them. People misjudge, mistype, troll, or take untested products of unknown strength. They are not a dose guide and never override the sourced table above. They exist only so the sourced ranges can be compared with what people say they take. If you are deciding what to take, use the sourced table, start low, and read the risks section.
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Duration

Route · sourceOnsetCome-upPeakOffsetTotalAfter-effects
Oral · PsychonautWiki15–45 minutes PW1–3 hours PW3–5 hours PW3–4 hours PW8–12 hours Up to 24h for irregular users. PW12–24 hours PW
Rectal · PsychonautWiki5–15 minutes PW3–5 minutes PW2–4 hours PW3–5 hours PW6–10 hours Up to 18h for irregular users. PW12–24 hours PW
Smoked · PsychonautWiki7–10 seconds PW5–10 seconds PW1–3 hours PW1–3 hours PW2–6 hours Up to 12h for irregular users. PW2–24 hours PW
Insufflated · PsychonautWiki3–5 minutes PW3–5 minutes PW1.5–3 hours PW2–4 hours PW4–7 hours Up to 12h for irregular users. PW6–24 hours PW
Intravenous · PsychonautWiki15–30 seconds PW1–2 minutes PW1–3 hours PW3–4 hours PW4–8 hours Up to 18h for irregular users. PW12–24 hours PW

TripSit factsheet

Onset
Insufflated: 5-10 minutes · Intravenous: 0-2 minutes · Oral: 20-70 minutes · Smoked: 0-2 minutes TS
Duration
Insufflated: 8-10 hours · Intravenous: 4-8 hours · Oral: 10-12 hours · Smoked: 3-8 hours TS
Aftereffects
24 hours TS

Mixing

Acute combinations: what happens when these are taken close together. Entries backed by a medical journal or agency are listed first.

Backed by medical journals

Awaiting sourcePeer-reviewed reports on acute combinations, from PubMed and the journals the harm reduction sites cite.

PsychonautWiki also lists dangerous combinations shared across a whole group (amphetamines) in a table this page does not copy. Read that list on PsychonautWiki.

TripSit combination chart

TripSit rates each pairing. Only pairings with a number carry a citation from TripSit. See the whole chart, with TripSit's note for every pairing.

Dangerous

amt TStramadol TS

Unsafe

dextromethorphan TSpcp TS

Caution

alcohol TScaffeine TScannabis TScocaine TSdmt TSketamine TSlsd TSmdma[19][20][21] TSmescaline TSmushrooms TSmxe TS

Low Risk & Synergy

nitrous TS

Risks and toxicity

Neurotoxicity

There is evidence that methamphetamine causes brain damage from long-term use in humans; 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.[22] PW

Unlike amphetamine, methamphetamine is directly neurotoxic to dopamine neurons. Moreover, methamphetamine abuse is associated with an increased risk of Parkinson's disease due to excessive pre-synaptic dopamine autoxidation, a mechanism of neurotoxicity. Similar to the neurotoxic effects on the dopamine system, methamphetamine can also result in neurotoxicity to serotonin neurons. It has been demonstrated that a high core temperature is correlated with an increase in the neurotoxic effects of methamphetamine. As a result of methamphetamine-induced neurotoxicity to dopamine neurons, chronic use may also lead to post acute withdrawals which persist beyond the withdrawal period for months, and even up to a year.[17][23–28] PW

Dependence and abuse potential

As with other stimulants, the chronic use of methamphetamine can be considered extremely addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage. PW

Tolerance to the effects of methamphetamine rapidly develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). Methamphetamine presents cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of methamphetamine all stimulants will have a reduced effect.[29][30] PW

The evidence on effective treatments for amphetamine and methamphetamine dependence and abuse is limited. In light of this, fluoxetine and imipramine appear to have some limited benefits in treating abuse and addiction, "no treatment has been demonstrated to be effective for the treatment of methamphetamine dependence and abuse".[31] PW

In highly dependent amphetamine and methamphetamine abusers, "when chronic heavy users abruptly discontinue methamphetamine use, many report a time-limited withdrawal syndrome that occurs within 24 hours of their last dose". Withdrawal symptoms in chronic, high-dose users are frequent, occurring in up to 87.6% of cases, and persist for three to four weeks with a marked "crash" phase occurring during the first week. Methamphetamine withdrawal symptoms can include anxiety, drug craving, dysphoric mood, fatigue, increased appetite, increased movement or decreased movement, lack of motivation, sleeplessness or sleepiness, and vivid or lucid dreams. Withdrawal symptoms are associated with the degree of dependence (i.e., the extent of abuse). The mental depression associated with methamphetamine withdrawal lasts longer and is more severe than that of cocaine withdrawal.[32][33] PW

Although it is clear that vaporised methamphetamine is more addictive than oral or insufflated amphetamine, there is debate as to whether the drug itself is inherently more addictive, and if so, how important the difference is. Besides the duration of action, the main difference between the two drugs is that methamphetamine is proportionally more centrally and less peripherally active. One reason is because the increased lipid solubility of the methyl group causes faster central absorption. Another cause is the fact that methamphetamine releases proportionally more dopamine at an equivalent dose. D-methamphetamine releases a dopamine:norepinephrine ratio of ~1:1.3 from synapses versus ~1:2 for d-amphetamine. Their effect on the norepinephrine (NET) and dopamine (DAT) transporters are more alike but there is a slight difference. D-methamphetamine favours NET by a factor of about 4 vs 5 for d-amphetamine. D-methamphetamine is also slightly more serotonergic. This may be a negligible difference, as the ratio of serotonin:norepinephrine release is only 1:60 for d-methamphetamine and 1:80 for d-amphetamine. Neither drug has any appreciable affinity for the serotonin transporter (SERT).[34] PW

This increased central vs peripheral effect of methamphetamine agrees with the common subjective feeling among stimulant users that the methamphetamine high has less of an inherently 'jittery' quality to it. The downside is that this aversive effect may be helpful as it discourages harmful levels of use. It is unclear what real world impact this difference has. A double-blind but small study of 13 methamphetamine users revealed only a minor preference towards methamphetamine, and this may be explained by the users having a greater familiarity with the drug.[35] PW

It is strongly recommended that one use harm reduction practices when using this substance. PW

Psychosis

Abuse of methamphetamine can result in a stimulant psychosis that may present with a variety of symptoms (e.g., paranoia, hallucinations, delusions). A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely. The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis. Psychosis very rarely arises from therapeutic use.[32][36][37] PW

Overdose

A methamphetamine overdose may result in a wide range of symptoms and is potentially fatal at heavy dosages. A moderate overdose of methamphetamine may induce symptoms such as abnormal heart rhythm, confusion, dysuria, high or low blood pressure, hyperthermia, hyperreflexia, myalgia, severe agitation, tachypnea, tremor, urinary hesitancy, and urinary retention. An extremely large overdose may produce symptoms such as adrenergic storm, methamphetamine psychosis, anuria, cardiogenic shock, cerebral hemorrhage, circulatory collapse, hyperpyrexia, pulmonary hypertension, renal failure, rhabdomyolysis, serotonin syndrome, and a form of stereotypy ("tweaking"). A methamphetamine overdose will likely also result in mild brain damage due to dopaminergic and serotonergic neurotoxicity. Death from fatal methamphetamine poisoning is typically preceded by convulsions and coma.[17][23][38][39] PW

Emergency treatment

Acute methamphetamine overdose is largely managed by treating the symptoms, and administration of benzodiazepines relieves symptoms such as agitation, hypertension, tachycardia, and seizure.[40] PW

Harm reduction

Studies have shown that N-acetylcysteine (NAC) can block the harmful neurotoxic effects of methamphetamine while preventing neurotransmitter depletion in rats and clinical trials in humans to treat methamphetamine dependence are currently underway. NAC may be effective for reducing the cravings and psychological dependence as well. NAC has a short half life and a sustained release formulation may be preferred for harm reduction purposes. Selenium has also been shown to protect the brain against meth induced neurotoxicity. However, it is worth noting that this data is preliminary and may not be applicable to humans.[41][42] PW

TripSit factsheet

Avoid
Rinsing mouth with mouthwash high in alcohol due to drying effects; using sugar filled chewing gum; usage within 14 days of MAOI.[3][4][5] TS

Testing

Marquis
Deep reddish orange - Dark reddish brown TS

Effects

increased energy/alertness, Decreased need for sleep, Increased sociability, mood lift, increase sexuality, Excessive talking, Decreased appetite, Weight loss, Sweating, Distrubed sleep patterns, Bruxia, Visual and audiotory hallucinations itchiness, agressiveness, moodiness, fatal kidney disorder, possible brain damage liver damage. TS

Overview

N-Methylamphetamine (also known as Methamphetamine, Ma, Meth, Glass, Ice, Shard, Crank, Tina, T, Tweak, Yaba, Shabu, and Crystal) is a classical stimulant substance of the amphetamine class. It is structurally related to amphetamine, however it crosses the blood-brain barrier more rapidly, due to its relatively high lipid solubility. It produces its effects by increasing levels of the neurotransmitters serotonin, dopamine, and norepinephrine in the brain.[1][2] PW

A fairly common and very strong CNS stimulant. It is sometimes prescribed in the form of desoxyn for ADHD and severe obesity. In low doses, methamphetamine can elevate mood, increase alertness, concentration, energy and reduces appetite. At higher doses, it can induce mania, psychosis and muscle degeneration among other issues. Tolerant users may report much higher doses than new users.[3][4][5] TS

Methamphetamine is a central nervous system (CNS) stimulant that is primarily used as a recreational or performance-enhancing drug and less commonly as a second-line treatment for attention deficit hyperactivity disorder (ADHD). It has also been researched as a potential treatment for traumatic brain injury. Methamphetamine was discovered in 1893 and exists as two enantiomers: levo-methamphetamine and dextro-methamphetamine. Methamphetamine properly refers to a specific chemical substance, the racemic free base, which is an equal mixture of levomethamphetamine and dextromethamphetamine in their pure amine forms, but the hydrochloride salt, commonly called crystal meth, is widely used. Methamphetamine is rarely prescribed over concerns involving its potential for misuse as an aphrodisiac and euphoriant, among other concerns, as well as the availability of other drugs with comparable effects and treatment efficacy such as dextroamphetamine and lisdexamfetamine. While pharmaceutical formulations of methamphetamine in the United States are labeled as methamphetamine hydrochloride, they contain dextromethamphetamine as the active ingredient. Dextromethamphetamine is a stronger CNS stimulant than levomethamphetamine.[6–10] WP

Both racemic methamphetamine and dextromethamphetamine are illicitly trafficked and sold owing to their potential for recreational use and ease of manufacture. The highest prevalence of illegal methamphetamine use occurs in parts of Asia and Oceania, and in the United States, where racemic methamphetamine and dextromethamphetamine are classified as Schedule II controlled substances. Levomethamphetamine is available as an over-the-counter (OTC) drug for use as an inhaled nasal decongestant in the United States and is seldom abused. Internationally, the production, distribution, sale, and possession of methamphetamine is restricted or banned in many countries, owing to its placement in schedule II of the United Nations Convention on Psychotropic Substances treaty. While dextromethamphetamine is a more potent drug, racemic methamphetamine is illicitly produced more often, owing to the relative ease of synthesis and regulatory limits of chemical precursor availability.[11][12] WP

The effects of methamphetamine are nearly identical to other substituted amphetamines. In low to moderate and therapeutic doses (5–25 mg orally), methamphetamine produces typical SNDRA effects and may elevate mood, increase alertness, concentration, and energy, reduce appetite, and promote weight loss. In overdose or during extended binges, it may induce psychosis, breakdown of skeletal muscle, seizures, and bleeding in the brain. Chronic high-dose use can precipitate unpredictable and rapid mood swings, stimulant psychosis (e.g., paranoia, hallucinations, delirium, and delusions), and aggression. Recreationally, methamphetamine's ability to increase energy has been reported to lift mood and increase sexual desire to such an extent that users are able to engage in sexual activity continuously for several days while binging the drug. Methamphetamine is known to possess a high abuse liability (a high likelihood that extratherapeutic use will lead to compulsive drug use) and high psychological dependence liability (a high likelihood that withdrawal symptoms will occur when methamphetamine use ceases). Discontinuing methamphetamine after heavy use may lead to a post-acute-withdrawal syndrome, which can persist for months beyond the typical withdrawal period. At high doses, like other substituted amphetamines, methamphetamine is neurotoxic to human midbrain dopaminergic neurons and, to a lesser extent, serotonergic neurons. Methamphetamine neurotoxicity causes adverse changes in brain structure and function, such as reductions in grey matter volume in several brain regions, as well as adverse changes in markers of metabolic integrity.[13–17] WP

Methamphetamine belongs to the substituted phenethylamine and substituted amphetamine chemical classes and as a drug acts as a serotonin–norepinephrine–dopamine releasing agent. It is related to the other dimethylphenethylamines as a positional isomer of these compounds, which share the common chemical formula C₁₀H₁₅N. WP⚠ Part of this sentence could not be copied from the source. Open the source to read it in full.

History

Awaiting sourceHistory and culture from Wikipedia or PsychonautWiki, with their citations.

Pharmacology

Pharmacodynamics

Methamphetamine has been identified as a potent full agonist of trace amine-associated receptor 1 (TAAR1), a G protein-coupled receptor (GPCR) that regulates brain catecholamine systems. Activation of TAAR1 increases cyclic adenosine monophosphate (cAMP) production and either completely inhibits or reverses the transport direction of the dopamine transporter (DAT), norepinephrine transporter (NET), and serotonin transporter (SERT). When methamphetamine binds to TAAR1, it triggers transporter phosphorylation via protein kinase A (PKA) and protein kinase C (PKC) signaling, ultimately resulting in the internalization or reverse function of monoamine transporters. Methamphetamine is also known to increase intracellular calcium, an effect which is associated with DAT phosphorylation through a Ca2+/calmodulin-dependent protein kinase (CAMK)-dependent signaling pathway, in turn producing dopamine efflux. TAAR1 has been shown to reduce the firing rate of neurons through direct activation of G protein-coupled inwardly-rectifying potassium channels. TAAR1 activation by methamphetamine in astrocytes appears to negatively modulate the membrane expression and function of EAAT2, a type of glutamate transporter.[66–76] WP

In addition to its effect on the plasma membrane monoamine transporters, methamphetamine inhibits synaptic vesicle function by inhibiting VMAT2, which prevents monoamine uptake into the vesicles and promotes their release. Methamphetamine binds to VMAT2 via the resperine site, in contrast to amphetamine, which appears to bind at the tetrabenazine site. This results in the outflow of monoamines from synaptic vesicles into the cytosol (intracellular fluid) of the presynaptic neuron, and their subsequent release into the synaptic cleft by the phosphorylated transporters. Other transporters that methamphetamine is known to inhibit are SLC22A3 and SLC22A5. SLC22A3 is an extraneuronal monoamine transporter that is present in astrocytes, and SLC22A5 is a high-affinity carnitine transporter.[67][77–80] WP

Methamphetamine is also an agonist of the alpha-2 adrenergic receptors and sigma receptors with a greater affinity for σ₁ than σ₂, and inhibits monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B). Sigma receptor activation by methamphetamine may facilitate its central nervous system stimulant effects and promote neurotoxicity within the brain. Dextromethamphetamine is a stronger psychostimulant, but levomethamphetamine has stronger peripheral effects, a longer half-life, and longer perceived effects among heavy substance users. At high doses, both enantiomers of methamphetamine can induce similar stereotypy and methamphetamine psychosis, but levomethamphetamine has shorter psychodynamic effects.[67][81–85] WP

Pharmacokinetics

The bioavailability of methamphetamine is 67% orally, 79% intranasally, 67 to 90% via inhalation (smoking), and 100% intravenously. Following oral administration, methamphetamine is well-absorbed into the bloodstream, with peak plasma methamphetamine concentrations achieved in approximately 3.13–6.3 hours post ingestion. Methamphetamine is also well absorbed following inhalation and following intranasal administration. Because of the high lipophilicity of methamphetamine due to its methyl group, it can readily move through the blood–brain barrier faster than other stimulants, where it is more resistant to degradation by monoamine oxidase. The amphetamine metabolite peaks at 10–24 hours. Methamphetamine is excreted by the kidneys, with the rate of excretion into the urine heavily influenced by urinary pH. When taken orally, 30–54% of the dose is excreted in urine as methamphetamine and 10–23% as amphetamine. Following IV doses, about 45% is excreted as methamphetamine and 7% as amphetamine. The elimination half-life of methamphetamine varies with a range of 5–30 hours, but it is on average 9 to 12 hours in most studies. The elimination half-life of methamphetamine does not vary by route of administration, but is subject to substantial interindividual variability.[14][24][40][86][87][88] WP

CYP2D6, dopamine β-hydroxylase, flavin-containing monooxygenase 3, butyrate-CoA ligase, and glycine N-acyltransferase are the enzymes known to metabolize methamphetamine or its metabolites in humans. The primary metabolites are amphetamine and 4-hydroxymethamphetamine; other minor metabolites include: 4-hydroxyamphetamine, 4-hydroxynorephedrine, 4-hydroxyphenylacetone, benzoic acid, hippuric acid, norephedrine, and phenylacetone, the metabolites of amphetamine. Among these metabolites, the active sympathomimetics are amphetamine, 4‑hydroxyamphetamine, 4‑hydroxynorephedrine, 4-hydroxymethamphetamine, and norephedrine. Methamphetamine is a CYP2D6 inhibitor.[87][89–92] WP

The main metabolic pathways involve aromatic para-hydroxylation, aliphatic alpha- and beta-hydroxylation, N-oxidation, N-dealkylation, and deamination. The known metabolic pathways include:[87][93][94][95] WP⚠ A diagram follows this text in the source and is not copied here. Open the source to see it.

Detection in biological fluids

Methamphetamine and amphetamine are often measured in urine or blood as part of a drug test for sports, employment, poisoning diagnostics, and forensics. Chiral techniques may be employed to help distinguish the source of the drug to determine whether it was obtained illicitly or legally via prescription or prodrug. Chiral separation is needed to assess the possible contribution of levomethamphetamine, which is an active ingredient in some OTC nasal decongestants, toward a positive test result. Dietary zinc supplements can mask the presence of methamphetamine and other drugs in urine.[96–103] WP

Chemistry

Formula
C10H15N PC
CAS number
7632-10-2 PC
Molar mass (g/mol)
149.23 PC
IUPAC name (computed by PubChem)
N-methyl-1-phenylpropan-2-amine PC
SMILES
CC(CC1=CC=CC=C1)NC PC
InChIKey
MYWUZJCMWCOHBA-UHFFFAOYSA-N PC
PubChem CID
1206

User reports

Erowid erowid.org

Listings

Erowid Experience Vault listing TS

Link as published on TripSit's factsheet.

Top stories
Awaiting sourceShort summaries of the most-read reports, each linked, saying only what the report says.

Bluelight bluelight.org

Listings
Awaiting sourceTrip report threads and this substance's discussion forum.
Top stories
Awaiting sourceShort summaries of the most-read reports, each linked, saying only what the report says.

Reddit reddit.com

Listings
Awaiting sourceTrip report posts and the relevant subreddits.
Top stories
Awaiting sourceShort summaries of the most-read reports, each linked, saying only what the report says.

Pop culture

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Add a reference

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References

  1. Harm reduction site Erowid Methamphetamine (Speed, Crank) Vault
  2. Journal / agency Barr, A. M., Panenka, W. J., MacEwan, G. W., Thornton, A. E., Lang, D. J., Honer, W. G., Lecomte, T. The need for speed: an update on methamphetamine addiction. Journal of Psychiatry and Neuroscience. September 2006
  3. Journal / agency Comparison of intranasal methamphetamine and d-amphetamine self-administration by humans
  4. Other Methamphetamine or desoxyn should not be used within 14 days of using a MAOI drug - Mosby's Dental Drug Reference Ninth Edition 2010
  5. Other Meth/desoxyn usage for long periods of time in children or people who have not finished growing will cause temporary suppression of weight and height growth - Mosby's Dental Drug Reference 9th Ed. 2010
  6. Other Methamphetamine is contracted from N-methylamphetamine. Synonyms and alternate spellings include: N-methylamphetamine, desoxyephedrine, Syndrox, Methedrine, and Desoxyn. Common slang names for methamphetamine include: meth, speed, crank, and shabu (also sabu and shabu-shabu) in Indonesia and the Philippines, and for the hydrochloride crystal, crystal meth, glass, shards, and ice, and, in Canada, hoot, Tina, and, in New Zealand, P/Pure
  7. Journal / agency Moszczynska A, Callan SP. Molecular, Behavioral, and Physiological Consequences of Methamphetamine Neurotoxicity: Implications for Treatment. The Journal of Pharmacology and Experimental Therapeutics. September 2017. doi:10.1124/jpet.116.238501 · PMID 28630283 · PMC11047030
  8. Journal / agency Rau T, Ziemniak J, Poulsen D. The neuroprotective potential of low-dose methamphetamine in preclinical models of stroke and traumatic brain injury. Progress in Neuro-psychopharmacology & Biological Psychiatry. January 2016. doi:10.1016/j.pnpbp.2015.02.013 · PMID 25724762
  9. Other Enantiomers are molecules that are mirror images of one another; they are structurally identical, but of the opposite orientation. Levomethamphetamine and dextromethamphetamine are also known as L-methamphetamine, (R)-methamphetamine, or levmetamfetamine (International Nonproprietary Name [INN]) and D-methamphetamine, (S)-methamphetamine, or metamfetamine (INN), respectively
  10. Other The medication package insert for Desoxyn lists the chemical name (S)-N,α-dimethylbenzeneethanamine hydrochloride, which explicitly identifies the compound as dextromethamphetamine (the S-enantiomer) with no stereochemical ambiguity
  11. Journal / agency Barkholtz HM, Hadzima R, Miles A. Pharmacology of R-(-)-Methamphetamine in Humans: A Systematic Review of the Literature. ACS Pharmacology & Translational Science. July 2023. doi:10.1021/acsptsci.3c00019 · PMID 37470013 · PMC10353062
  12. Other The active ingredient in some OTC inhalers in the United States is listed as levmetamfetamine, the INN and USAN of levomethamphetamine
  13. Journal / agency Hart CL, Marvin CB, Silver R, Smith EE. Is cognitive functioning impaired in methamphetamine users? A critical review. Neuropsychopharmacology. February 2012. doi:10.1038/npp.2011.276 · PMID 22089317 · PMC3260986
  14. Journal / agency Desoxyn- methamphetamine hydrochloride tablet. 8 September 2022
  15. Other Meth's aphrodisiac effect adds to drug's allure. 3 December 2004
  16. Journal / agency Yu S, Zhu L, Shen Q, Bai X, Di X. Recent advances in methamphetamine neurotoxicity mechanisms and its molecular pathophysiology. Behavioural Neurology. March 2015. doi:10.1155/2015/103969 · PMID 25861156 · PMC4377385
  17. Journal / agency Krasnova IN, Cadet JL. Methamphetamine toxicity and messengers of death. Brain Res. Rev. May 2009. doi:10.1016/j.brainresrev.2009.03.002 · PMID 19328213 · PMC2731235
  18. Other Methamphetamine - City Vision
  19. Journal / agency Kelly J. Clemens, Iain S. McGregor, Glenn E. Hunt, Jennifer L. Cornish. MDMA, methamphetamine and their combination: possible lessons for party drug users from recent preclinical research
  20. Journal / agency Kelly J. Clemens, Iain S. McGregor, Glenn E. Hunt, Jennifer L. Cornish. Repeated weekly exposure to MDMA, methamphetamine or their combination: long-term behavioural and neurochemical effects in rats
  21. Journal / agency P. Leon Brown, Eugene A. Kiyatkin. Brain hyperthermia induced by MDMA (‘ecstasy’): modulation by environmental conditions
  22. Journal / agency Nie, L., Zhao, Z., Wen, X., Luo, W., Ju, T., Ren, A., Wu, B., Li, J. Gray-matter structure in long-term abstinent methamphetamine users. BMC psychiatry. 10 April 2020. doi:10.1186/s12888-020-02567-3
  23. Other Nestler, E. J., Hyman, S. E., Malenka, R. C. Molecular neuropharmacology: a foundation for clinical neuroscience. 2009
  24. Journal / agency Cruickshank, C. C., Dyer, K. R. A review of the clinical pharmacology of methamphetamine. Addiction (Abingdon, England). July 2009. doi:10.1111/j.1360-0443.2009.02564.x
  25. Journal / agency Thrash, B., Thiruchelvan, K., Ahuja, M., Suppiramaniam, V., Dhanasekaran, M. Methamphetamine-induced neurotoxicity: the road to Parkinson’s disease. Pharmacological Reports. November 2009. doi:10.1016/S1734-1140(09)70158-6
  26. Journal / agency Sulzer, D., Zecca, L. Intraneuronal dopamine-quinone synthesis: a review. Neurotoxicity Research. February 2000. doi:10.1007/BF03033289
  27. Journal / agency Miyazaki, I., Asanuma, M. Dopaminergic neuron-specific oxidative stress caused by dopamine itself. Acta Medica Okayama. June 2008. doi:10.18926/AMO/30942
  28. Journal / agency Yuan, J., Hatzidimitriou, G., Suthar, P., Mueller, M., McCann, U., Ricaurte, G. Relationship between temperature, dopaminergic neurotoxicity, and plasma drug concentrations in methamphetamine-treated squirrel monkeys. The Journal of Pharmacology and Experimental Therapeutics. March 2006. doi:10.1124/jpet.105.096503
  29. Journal / agency Pérez-Mañá, C., Castells, X., Torrens, M., Capellà, D., Farre, M. Efficacy of psychostimulant drugs for amphetamine abuse or dependence. The Cochrane Database of Systematic Reviews. 2 September 2013. doi:10.1002/14651858.CD009695.pub2
  30. Other http://www.merckmanuals.com/home/special_subjects/drug_use_and_abuse/amphetamines.html
  31. Journal / agency Srisurapanont, M., Jarusuraisin, N., Kittirattanapaiboon, P. Treatment for amphetamine dependence and abuse. The Cochrane Database of Systematic Reviews. 2001. doi:10.1002/14651858.CD003022
  32. Journal / agency Shoptaw, S. J., Kao, U., Heinzerling, K., Ling, W. Treatment for amphetamine withdrawal. The Cochrane Database of Systematic Reviews. 15 April 2009. doi:10.1002/14651858.CD003021.pub2
  33. Journal / agency Winslow, B. T., Voorhees, K. I., Pehl, K. A. Methamphetamine abuse. American Family Physician. 15 October 2007
  34. Wikipedia https://en.wikipedia.org/wiki/Monoamine_releasing_agent#Activity_profiles
  35. Journal / agency Kirkpatrick, M. G., Gunderson, E. W., Johanson, C.-E., Levin, F. R., Foltin, R. W., Hart, C. L. Comparison of intranasal methamphetamine and d-amphetamine self-administration by humans. Addiction (Abingdon, England). April 2012. doi:10.1111/j.1360-0443.2011.03706.x
  36. Other Hofmann, F. G. A handbook on drug and alcohol abuse: the biomedical aspects. 1983
  37. Journal / agency http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf
  38. Journal / agency Desoxyn Prescribing Information
  39. Other Goodman & Gilman’s pharmacological basis of therapeutics. 2011
  40. Journal / agency Robin, S., Michael, B. The clinical toxicology of metamfetamine. Clinical Toxicology. 2010. doi:10.3109/15563650.2010.516752
  41. Journal / agency Fukami, G., Hashimoto, K., Koike, K., Okamura, N., Shimizu, E., Iyo, M. Effect of antioxidant N-acetyl-l-cysteine on behavioral changes and neurotoxicity in rats after administration of methamphetamine. Brain Research. July 2004. doi:10.1016/j.brainres.2004.04.072
  42. Journal / agency Imam, S. Z., Newport, G. D., Islam, F., Slikker, W., Ali, S. F. Selenium, an antioxidant, protects against methamphetamine-induced dopaminergic neurotoxicity. Brain Research. 13 February 1999. doi:10.1016/S0006-8993(98)01311-0
  43. Harm reduction site http://www.unodc.org/pdf/youthnet/ATS.pdf
  44. Other http://web.archive.org/web/20051205125434/http://www.incb.org/pdf/e/list/green.pdf
  45. Other Health. Poisons Standard February 2019
  46. Other https://www.health.act.gov.au/about-our-health-system/population-health/drug-law-reform
  47. Other Suchtgiftverordnung
  48. Other https://www.in.gov.br/en/web/dou/-/resolucao-rdc-n-804-de-24-de-julho-de-2023-498447451
  49. Other Controlled Drugs and Substances Act - SCHEDULE I
  50. Other https://www.zakonyprolidi.cz/cs/2013-463
  51. Other Arrêté du 22 février 1990 fixant la liste des substances classées comme stupéfiants
  52. Other The Nazi Death Machine: Hitler's Drugged Soldiers. May 6, 2005
  53. Other Anlage II BtMG
  54. Other Einundzwanzigste Verordnung zur Änderung betäubungsmittelrechtlicher Vorschriften
  55. Other § 29 BtMG
  56. Harm reduction site UNODC - Bulletin on Narcotics - 1957 Issue 3 - 002
  57. Other Opiumwet
  58. Other Schedule 1 - Class A controlled drugs
  59. Other Ustawa z dnia 24 kwietnia 2015 r. o zmianie ustawy o przeciwdziałaniu narkomanii oraz niektórych innych ustaw (Dz.U. z 2015 r. poz. 875)
  60. Other https://web.archive.org/web/20160331074842/https://treaties.un.org/pages/ViewDetails.aspx?src=TREATY&mtdsg_no=VI-16&chapter=6&lang=en
  61. Other https://www.lakemedelsverket.se/sv/lagar-och-regler/foreskrifter/2011-10-konsoliderad
  62. Other Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien
  63. Other Corporate report - Controlled Drugs
  64. Journal / agency Controlled Drugs and Substances Act
  65. Other List of psychotropic substances under international control. August 2003
  66. Journal / agency Miller GM. The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity. J. Neurochem. January 2011. doi:10.1111/j.1471-4159.2010.07109.x · PMID 21073468 · PMC3005101
  67. Harm reduction site Methamphetamine: Targets. 8 February 2013
  68. Journal / agency Borowsky B, Adham N, Jones KA, Raddatz R, Artymyshyn R, Ogozalek KL, Durkin MM, Lakhlani PP, Bonini JA, Pathirana S, Boyle N, Pu X, Kouranova E, Lichtblau H, Ochoa FY, Branchek TA, Gerald C. Trace amines: identification of a family of mammalian G protein-coupled receptors. Proc. Natl. Acad. Sci. U.S.A. July 2001. doi:10.1073/pnas.151105198 · PMID 11459929 · PMC55357
  69. Journal / agency Xie Z, Miller GM. A receptor mechanism for methamphetamine action in dopamine transporter regulation in brain. J. Pharmacol. Exp. Ther. July 2009. doi:10.1124/jpet.109.153775 · PMID 19364908 · PMC2700171
  70. Other Maguire JJ, Davenport AP. TA₁ receptor. 2 December 2014
  71. Journal / agency Underhill SM, Wheeler DS, Li M, Watts SD, Ingram SL, Amara SG. Amphetamine modulates excitatory neurotransmission through endocytosis of the glutamate transporter EAAT3 in dopamine neurons. Neuron. July 2014. doi:10.1016/j.neuron.2014.05.043 · PMID 25033183 · PMC4159050
  72. Journal / agency Vaughan RA, Foster JD. Mechanisms of dopamine transporter regulation in normal and disease states. Trends Pharmacol. Sci. September 2013. doi:10.1016/j.tips.2013.07.005 · PMID 23968642 · PMC3831354
  73. Journal / agency Ledonne A, Berretta N, Davoli A, Rizzo GR, Bernardi G, Mercuri NB. Electrophysiological effects of trace amines on mesencephalic dopaminergic neurons. Front. Syst. Neurosci. July 2011. doi:10.3389/fnsys.2011.00056 · PMID 21772817 · PMC3131148
  74. Other mct. TAAR1. 28 January 2012
  75. Journal / agency Revel FG, Moreau JL, Gainetdinov RR, Bradaia A, Sotnikova TD, Mory R, Durkin S, Zbinden KG, Norcross R, Meyer CA, Metzler V, Chaboz S, Ozmen L, Trube G, Pouzet B, Bettler B, Caron MG, Wettstein JG, Hoener MC. TAAR1 activation modulates monoaminergic neurotransmission, preventing hyperdopaminergic and hypoglutamatergic activity. Proc. Natl. Acad. Sci. U.S.A. May 2011. doi:10.1073/pnas.1103029108 · PMID 21525407 · PMC3101002
  76. Journal / agency Cisneros IE, Ghorpade A. Methamphetamine and HIV-1-induced neurotoxicity: role of trace amine associated receptor 1 cAMP signaling in astrocytes. Neuropharmacology. October 2014. doi:10.1016/j.neuropharm.2014.06.011 · PMID 24950453 · PMC4315503
  77. Harm reduction site Methamphetamine: Transporters. 8 February 2013
  78. Journal / agency Sulzer D, Sonders MS, Poulsen NW, Galli A. Mechanisms of neurotransmitter release by amphetamines: a review. Progress in Neurobiology. April 2005. doi:10.1016/j.pneurobio.2005.04.003 · PMID 15955613
  79. Journal / agency Eiden LE, Weihe E. VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse. Ann. N. Y. Acad. Sci. January 2011. doi:10.1111/j.1749-6632.2010.05906.x · PMID 21272013 · PMC4183197
  80. Journal / agency Inazu M, Takeda H, Matsumiya T. The role of glial monoamine transporters in the central nervous system. Nihon Shinkei Seishin Yakurigaku Zasshi. August 2003. PMID 13677912
  81. Journal / agency Kaushal N, Matsumoto RR. Role of sigma receptors in methamphetamine-induced neurotoxicity. Curr Neuropharmacol. March 2011. doi:10.2174/157015911795016930 · PMID 21886562 · PMC3137201
  82. Journal / agency Rodvelt KR, Miller DK. Could sigma receptor ligands be a treatment for methamphetamine addiction?. Curr Drug Abuse Rev. September 2010. doi:10.2174/1874473711003030156 · PMID 21054260
  83. Journal / agency Melega WP, Cho AK, Schmitz D, Kuczenski R, Segal DS. l-methamphetamine pharmacokinetics and pharmacodynamics for assessment of in vivo deprenyl-derived l-methamphetamine. J. Pharmacol. Exp. Ther. February 1999. doi:10.1016/S0022-3565(24)38016-4 · PMID 9918585
  84. Journal / agency Kuczenski R, Segal DS, Cho AK, Melega W. Hippocampus norepinephrine, caudate dopamine and serotonin, and behavioral responses to the stereoisomers of amphetamine and methamphetamine. J. Neurosci. February 1995. doi:10.1523/jneurosci.15-02-01308.1995 · PMID 7869099 · PMC6577819
  85. Journal / agency Mendelson J, Uemura N, Harris D, Nath RP, Fernandez E, Jacob P, Everhart ET, Jones RT. Human pharmacology of the methamphetamine stereoisomers. Clin. Pharmacol. Ther. October 2006. doi:10.1016/j.clpt.2006.06.013 · PMID 17015058
  86. Journal / agency Courtney KE, Ray LA. Methamphetamine: an update on epidemiology, pharmacology, clinical phenomenology, and treatment literature. Drug Alcohol Depend. October 2014. doi:10.1016/j.drugalcdep.2014.08.003 · PMID 25176528 · PMC4164186
  87. Harm reduction site Methamphetamine: Pharmacology. 2 October 2017
  88. Journal / agency Xu J, Zhang Z, Liu R, Sun Y, Liu H, Nie Z, Zhao X, Pu X. Function of complement factor H and imaging of small molecules by MALDI-MSI in a methamphetamine behavioral sensitization model. Behavioural Brain Research. May 2019. doi:10.1016/j.bbr.2019.02.002 · PMID 30731099
  89. Journal / agency p-Hydroxyamphetamine: Compound Summary
  90. Journal / agency p-Hydroxynorephedrine: Compound Summary
  91. Journal / agency Phenylpropanolamine: Compound Summary
  92. Harm reduction site Methamphetamine: Enzymes. 8 February 2013
  93. Journal / agency Amphetamine
  94. Journal / agency Haiser HJ, Turnbaugh PJ. Developing a metagenomic view of xenobiotic metabolism. Pharmacol. Res. March 2013. doi:10.1016/j.phrs.2012.07.009 · PMID 22902524 · PMC3526672
  95. Journal / agency Caldwell J, Hawksworth GM. The demethylation of methamphetamine by intestinal microflora. The Journal of Pharmacy and Pharmacology. May 1973. doi:10.1111/j.2042-7158.1973.tb10043.x · PMID 4146404
  96. Journal / agency Liddle DG, Connor DJ. Nutritional supplements and ergogenic AIDS. Prim. Care. June 2013. doi:10.1016/j.pop.2013.02.009 · PMID 23668655
  97. Journal / agency Kraemer T, Maurer HH. Determination of amphetamine, methamphetamine and amphetamine-derived designer drugs or medicaments in blood and urine. J. Chromatogr. B. August 1998. doi:10.1016/S0378-4347(97)00515-X · PMID 9700558
  98. Journal / agency Kraemer T, Paul LD. Bioanalytical procedures for determination of drugs of abuse in blood. Anal. Bioanal. Chem. August 2007. doi:10.1007/s00216-007-1271-6 · PMID 17468860
  99. Journal / agency Goldberger BA, Cone EJ. Confirmatory tests for drugs in the workplace by gas chromatography-mass spectrometry. J. Chromatogr. A. July 1994. doi:10.1016/0021-9673(94)85218-9 · PMID 8075776
  100. Journal / agency Paul BD, Jemionek J, Lesser D, Jacobs A, Searles DA. Enantiomeric separation and quantitation of (+/-)-amphetamine, (+/-)-methamphetamine, (+/-)-MDA, (+/-)-MDMA, and (+/-)-MDEA in urine specimens by GC-EI-MS after derivatization with (R)-(−)- or (S)-(+)-alpha-methoxy-alpha-(trifluoromethy)phenylacetyl chloride (MTPA). J. Anal. Toxicol. September 2004. doi:10.1093/jat/28.6.449 · PMID 15516295
  101. Journal / agency de la Torre R, Farré M, Navarro M, Pacifici R, Zuccaro P, Pichini S. Clinical pharmacokinetics of amfetamine and related substances: monitoring in conventional and non-conventional matrices. Clin Pharmacokinet. 2004. doi:10.2165/00003088-200443030-00002 · PMID 14871155
  102. Other Baselt RC. Disposition of toxic drugs and chemicals in man. 2020
  103. Journal / agency Venkatratnam A, Lents NH. Zinc reduces the detection of cocaine, methamphetamine, and THC by ELISA urine testing. J. Anal. Toxicol. July 2011. doi:10.1093/anatox/35.6.333 · PMID 21740689

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