Methamphetamine
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Collated from PsychonautWiki, TripSit, Pharmacology, DrugCentral. Where sources differ (e.g. dosing), Compare shows them side by side.
Also known as Methamphetamine, Meth, Crystal, Desoxyn, Speed, Ma, Ice, Glass, Shard, Tina, T, Tweak, Crank, Shabu, Yaba, tikPW
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.TS
Insufflated
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 5 mg | 5–10 mg | 10–30 mg | 30–60 mg | 60 mg+ |
| Onset | 3–5 minutes |
|---|---|
| Come-up | 3–5 minutes |
| Peak | 1.5–3 hours |
| Offset | 2–4 hours |
| Total | 4–7 hours |
| After-effects | 6–24 hours |
Intravenous
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 5 mg | 5–10 mg | 10–30 mg | 30–40 mg | 40 mg+ |
| Onset | 15–30 seconds |
|---|---|
| Come-up | 1–2 minutes |
| Peak | 1–3 hours |
| Offset | 3–4 hours |
| Total | 4–8 hours |
| After-effects | 12–24 Hours |
Oral
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 5 mg | 5–10 mg | 10–25 mg | 25–50 mg | 50 mg+ |
| Onset | 15–45 minutes |
|---|---|
| Come-up | 1–3 hours |
| Peak | 3–5 hours |
| Offset | 3–4 hours |
| Total | 8–12 hours |
| After-effects | 12–24 hours |
Rectal
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 5 mg | 5–10 mg | 10–30 mg | 30–40 mg | 40 mg+ |
| Onset | 5–15 minutes |
|---|---|
| Come-up | 3–5 minutes |
| Peak | 2–4 hours |
| Offset | 3–5 hours |
| Total | 6–10 hours |
| After-effects | 12–24 hours |
Smoked
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 5 mg | 5–10 mg | 10–20 mg | 20–60 mg | 60 mg+ |
| Onset | 7–10 seconds |
|---|---|
| Come-up | 5–10 seconds |
| Peak | 1–3 hours |
| Offset | 1–3 hours |
| Total | 2–6 hours |
| After-effects | 2–24 hours |
Caution / uncertainPW
🧬 Receptor activityPHDC
| Target | Action | Affinity | Source | |
|---|---|---|---|---|
| Synaptic vesicular amine transporter | — | Ki 2460 nM | CHEMBL | TargetSynaptic vesicular amine transporter Action— AffinityKi 2460 nM SourceCHEMBL |
| Sigma non-opioid intracellular receptor 1 | — | Ki 8320 nM | CHEMBL | TargetSigma non-opioid intracellular receptor 1 Action— AffinityKi 8320 nM SourceCHEMBL |
| Amine oxidase [flavin-containing] B | — | Ki 270000 nM | CHEMBL | TargetAmine oxidase [flavin-containing] B Action— AffinityKi 270000 nM SourceCHEMBL |
| Sodium-dependent dopamine transporter (SLC6A3) | Inhibitor | 7.611 Ki | DRUGCENTRAL | TargetSodium-dependent dopamine transporter (SLC6A3) ActionInhibitor Affinity7.611 Ki SourceDRUGCENTRAL |
| Sodium-dependent noradrenaline transporter (SLC6A2) | Inhibitor | 7.91 Ki | DRUGCENTRAL | TargetSodium-dependent noradrenaline transporter (SLC6A2) ActionInhibitor Affinity7.91 Ki SourceDRUGCENTRAL |
| Sodium-dependent serotonin transporter (SLC6A4) | Inhibitor | 6.133 Ki | DRUGCENTRAL | TargetSodium-dependent serotonin transporter (SLC6A4) ActionInhibitor Affinity6.133 Ki SourceDRUGCENTRAL |
| Trace amine-associated receptor 1 (TAAR1) | Agonist | 5.89 EC50 | DRUGCENTRAL | TargetTrace amine-associated receptor 1 (TAAR1) ActionAgonist Affinity5.89 EC50 SourceDRUGCENTRAL |
| 5-hydroxytryptamine receptor 2B (HTR2B) | — | 5 Ki | DRUGCENTRAL | Target5-hydroxytryptamine receptor 2B (HTR2B) Action— Affinity5 Ki SourceDRUGCENTRAL |
| Alpha-2A adrenergic receptor (ADRA2A) | — | 5.383 Ki | DRUGCENTRAL | TargetAlpha-2A adrenergic receptor (ADRA2A) Action— Affinity5.383 Ki SourceDRUGCENTRAL |
| Alpha-2B adrenergic receptor (ADRA2B) | — | 6.128 Ki | DRUGCENTRAL | TargetAlpha-2B adrenergic receptor (ADRA2B) Action— Affinity6.128 Ki SourceDRUGCENTRAL |
| Alpha-2C adrenergic receptor (ADRA2C) | — | 6.09 Ki | DRUGCENTRAL | TargetAlpha-2C adrenergic receptor (ADRA2C) Action— Affinity6.09 Ki SourceDRUGCENTRAL |
| Sigma non-opioid intracellular receptor 1 (SIGMAR1) | — | 5.08 Ki | DRUGCENTRAL | TargetSigma non-opioid intracellular receptor 1 (SIGMAR1) Action— Affinity5.08 Ki SourceDRUGCENTRAL |
| Synaptic vesicular amine transporter (Slc18a2) | — | 5.61 Ki | DRUGCENTRAL | TargetSynaptic vesicular amine transporter (Slc18a2) Action— Affinity5.61 Ki SourceDRUGCENTRAL |
| Trace amine-associated receptor 1 (TAAR1) | — | 5.28 EC50 | DRUGCENTRAL | TargetTrace amine-associated receptor 1 (TAAR1) Action— Affinity5.28 EC50 SourceDRUGCENTRAL |
Mechanism of actionPH
Methamphetamine enters the brain and triggers a cascading release of norepinephrine, dopamine and serotonin. To a lesser extent methamphetamine acts as a dopaminergic and adrenergic reuptake inhibitor and in high concentrations as a monamine oxidase inhibitor (MAOI). The mechanism of action involved in producing the beneficial behavioral changes seen in hyperkinetic children receiving methamphetamine is unknown.
Appears to exert most or all of its effect in the CNS by causing release of biogenic amines, especialy norepinephrine and dopamine, from storage sites in nerve terminals. It may also slow down catecholamine metabolism by inhibiting monoamine oxidase. The toxic effects of methamphetamine on dopamine and serotonergic neurons have recently been linked to the endogenous formation of c-hydroxy dopamine and 5, 7 dihydrotryptamine, respectively. The ability of methamphetamine to both release dopamine and serotonin as well as to inhibit monoamine oxidase activity leads to the non-enzymatic oxidation of dopamine and serotonin. Methamphetamine induced neuronal damage is mediated by the production of free radicals. This drug causes a long lasting depletion of dopamine and serotonin in the striatum and that pre-treatment alteration of this effect by four different antioxidants, as well as an inhibitor of superoxidase dismutase, indicate that oxygen free radicals have a role in methamphetamine induced neurotoxicity.
PharmacodynamicsPH
Methamphetamine is a potent central nervous system stimulant which affects neurochemical mechanisms responsible for regulating heart rate, body temperature, blood pressure, appetite, attention, mood and responses associated with alertness or alarm conditions. The acute effects of the drug closely resemble the physiological and psychological effects of an epinephrine-provoked fight-or-flight response, including increased heart rate and blood pressure, vasoconstriction (constriction of the arterial walls), bronchodilation, and hyperglycemia (increased blood sugar). Users experience an increase in focus, increased mental alertness, and the elimination of fatigue, as well as a decrease in appetite.
Pharmacokinetics
Half-lifePH
The biological half-life has been reported in the range of 4 to 5 hours.
The biologic half-life of methamphetamine reportedly is 4-5 hours.
AbsorptionPH
Methamphetamine is rapidly absorbed from the gastrointestinal tract with peak methamphetamine concentrations occurring in 3.13 to 6.3 hours post ingestion. Moreover, when administered intranasally or as an inhalation, methamphetamine also demonstrates a high degree of absorption. It is distributed to most parts of the body. Because methamphetamine has a high lipophilicity it is distributed across the blood brain barrier and crosses the placenta.
Excretion occurs primarily in the urine, the rate of which is dependent on urine pH. Between 30-54% of an oral dose is excreted in urine as unchanged methamphetamine and 10-23% as unchanged amphetamine. Following an intravenous dose, 45% is excreted as unchanged parent drug and 7% amphetamine.
Methamphetamine is readily absorbed from the GI tract and effects persist for 6-12 hours but may continue up to 24 hr after large doses. /Methamphetamine hydrochloride/
Single pharmacological doses of amphetamines (ie, 10-25 mg) given to human volunteers produce peak plasma levels within 1-2 hr & are rapidly absorbed from the GI tract. Amphetamine absorption usually is complete by 4-6 hr. The illicit use of amphetamines ... by insertion into the vagina (termed "balling") before intercourse suggests that these compounds are also absorbed through mucosal surfaces. ... Methamphetamine ... /has/ absorption characteristics similar to those of amphetamines. ... Sustained release prepn are avail as resin-bound rather than soluble salts. These compounds display reduced peak blood levels compared with std amphetamine prepn, but total bioavailability & time to peak levels remain similar. Pharmacokinetics in overdose are not well described.
Methamphetamine is eliminated principally in urine. Urinary excretion of the drug is pH dependent, and excretion is enhanced in acidic urine. Following oral administration of methamphetamine hydrochloride, approximately 62% of the administered dose is excreted in urine within the first 24 hours, with metabolites and unchanged drug accounting for about two-thirds and one-third, respectively, of the recovered drug.
Methamphetamine hydrochloride has been measured in human sweat at a median range of 63.0 (low dose 16.8-175) and 307 (high dose 199-607) ng per patch(1). /Methamphetamine hydrochloride/
MetabolismPH
Hepatic. The primary site of metabolism is in the liver by aromatic hydroxylation, N-dealkylation and deamination. At least seven metabolites have been identified in the urine, with the main metabolites being amphetamine (active) and 4-hydroxymethamphetamine. Other minor metabolites include 4-hydroxyamphetamine, norephedrine, and 4-hydroxynorephedrine.
Methamphetamine is metabolized in the liver by aromatic hydroxylation, N-dealkylation, and deamination; at least 7 metabolites have been identified in urine.
A species difference was found in a study of the metabolism of methamphetamine, (+/-)-2-methylamino-1-phenylpropane. In man, 22% of an oral dose was excreted into urine unchanged, & 15% of the dose was excreted as 4-hydroxymethamphetamine. After ip admin to rat, 4-hydroxymethamphetamine was principal urinary metabolite (31% of dose), together with 4-hydroxynorephedrine (16%) & unchanged drug (11% of dose). In the guinea pig an ip dose was extensively metabolized to benzoic acid & its glycine & glucuronic acid conjugates.
In vivo metab of N-alkylated amphetamines in rat produced 4-hydroxy- & 4-hydroxy-3-methoxy-metabolites. Relative quantities of phenolic metabolites formed were dependent upon the length of the N-alkyl substituent.
Metamphetamine has known human metabolites that include Amphetamine and 4-Hydroxymethamphetamine.
Hepatic. The primary site of metabolism is in the liver by aromatic hydroxylation, N-dealkylation and deamination. At least seven metabolites have been identified in the urine, with the main metabolites being amphetamine (active) and 4-hydroxymethamphetamine. Other minor metabolites include 4-hydroxyamphetamine, norephedrine, and 4-hydroxynorephedrine.
Route of Elimination: Excretion occurs primarily in the urine, the rate of which is dependent on urine pH. Between 30-54% of an oral dose is excreted in urine as unchanged methamphetamine and 10-23% as unchanged amphetamine. Following an intravenous dose, 45% is excreted as unchanged parent drug and 7% amphetamine.
Half Life: The biological half-life has been reported in the range of 4 to 5 hours.
Plan a dose of Methamphetamine
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Fact-sheets from PsychonautWiki. Harm-reduction reference only — not medical advice.