Methamphetamin

DEA NFLIS-Drug Category -> Phenethylamines (Amphetamines) (S)

Pharmaceuticals -> Illicit drugs

Pharmaceuticals -> Synthetic Cannabinoids or Psychoactive Compounds

Pharmaceuticals -> Listed in ZINC15

log Kow = 2.07

2.07

Characteristic odor resembling geranium leaves

Odorless

Clear, colorless liquid

White crystalline powder

In water, 0.5 g/mL

Soluble in ethanol, diethyl ether

Miscible with chloroform

9.28e-01 g/L

Breast Feeding; Lactation; Milk, Human; Street Drugs; Sympathomimetics; Dopamine Agents; Central Nervous System Stimulants; Adrenergic Agents; Wakefulness-Promoting Agents

Pharmaceuticals

Danger

H301 (97.6%): Toxic if swallowed [Danger Acute toxicity, oral]

P264, P270, P301+P316, P321, P330, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 42 reports by companies from 3 notifications to the ECHA C&L Inventory.

Danger

H225: Highly Flammable liquid and vapor [Danger Flammable liquids]

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including methamphetamine hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Methamphetamine hydrochloride/

Schedule II shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... (d) Stimulants. Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation which contains any quantity of the following substances having a stimulant effect on the central nervous system: Methamphetamine, its salts, isomers, and salts of its isomers (DEA Code Number: 1105) is included on this list. /Methamphetamine, its salts, isomers, and salts of its isomers/

DHHS/NIDA; Research Monograph Series 52: Testing Drugs for Physical Dependence Potential and Abuse Liability (1984) DHHS Pub No. (ADM)87-1332

DHHS/NIDA; Research Monograph Series 54: Mechanisms of Tolerance and Dependence (1984) DHHS Pub No. (ADM)88-1330

DHHS/NIDA; Research Monograph Series 56: Etiology of Drug Abuse: Implications for Prevention (1987) DHHS Pub No. (ADM)87-1335

DHHS/NIDA; Research Monograph Series 59: Current Research on the Consequences of Maternal Drug Abuse (1985) DHHS Pub No. (ADM)85-1400

For more Special Reports (Complete) data for d-METHAMPHETAMINE (8 total), please visit the HSDB record page.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Conditions for safe storage, including any incompatibilities: Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage. Recommended storage temperature -20 °C

ACCIDENTAL RELEASE MEASURES. Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid breathing vapours, mist or gas. Ensure adequate ventilation. Remove all sources of ignition. Evacuate personnel to safe areas. Beware of vapours accumulating to form explosive concentrations. Vapours can accumulate in low areas.; Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains.; Methods and materials for containment and cleaning up: Contain spillage, and then collect with an electrically protected vacuum cleaner or by wet-brushing and place in container for disposal according to local regulations.

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

Appropriate engineering controls: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid inhalation of vapour or mist. Use explosion-proof equipment.Keep away from sources of ignition - No smoking.Take measures to prevent the build up of electrostatic charge.

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multipurpose combination (US) or type ABEK (EN 14387) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Body Protection: Complete suit protecting against chemicals, Flame retardant antistatic protective clothing., The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Skin protection: Handle with gloves.

Eye/face protection: Face shield and safety glasses Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Management of acute methamphetamine intoxication is largely symptomatic and includes gastric evacuation, administration of activated charcoal, and sedation. Experience with hemodialysis or peritoneal dialysis is inadequate to permit recommendations in this regard. Acidification of urine increases methamphetamine excretion, but is believed to increase risk of acute renal failure if myoglobinuria is present. Intravenous phentolamine has been suggested for possible acute, severe hypertension, if this complicates methamphetamine overdosage. Usually a gradual drop in blood pressure will result when sufficient sedation has been achieved. Chlorpromazine has been reported to be useful in decreasing CNS stimulation and sympathomimetic effects. (L1712)

BACKGROUND: Methamphetamine addiction is a significant public health problem for which no Food and Drug Administration-approved pharmacotherapies exist. Preclinical drug vs. food choice procedures have been predictive of clinical medication efficacy in the treatment of opioid and cocaine addiction. Whether preclinical choice procedures are predictive of candidate medication effects for other abused drugs, such as methamphetamine, remains unclear. The present study aim was to determine continuous 7-day treatment effects with the monoamine releaser d-amphetamine and the monoamine uptake inhibitor methylphenidate on methamphetamine vs. food choice. In addition, 7-day cocaine treatment effects were also examined. METHODS: Behavior was maintained under a concurrent schedule of food delivery (1-g pellets, fixed-ratio 100 schedule) and methamphetamine injections (0-0.32mg/kg/injection, fixed-ratio 10 schedule) in male rhesus monkeys (n=4). Methamphetamine choice dose-effect functions were determined daily before and during 7-day periods of continuous intravenous treatment with d-amphetamine (0.01-0.1mg/kg/hr), methylphenidate (0.032-0.32mg/kg/hr), or cocaine (0.1-0.32mg/kg/hr). RESULTS: During saline treatment, increasing methamphetamine doses resulted in a corresponding increase in methamphetamine vs. food choice. Continuous 7-day treatments with d-amphetamine, methylphenidate or cocaine did not significantly attenuate methamphetamine vs. food choice up to doses that decreased rates of operant responding. However, 0.1mg/kg/hr d-amphetamine did eliminate methamphetamine choice in two monkeys. CONCLUSIONS: The present subchronic treatment results support the utility of preclinical methamphetamine choice to evaluate candidate medications for methamphetamine addiction. Furthermore, these results confirm and extend previous results demonstrating differential pharmacological mechanisms between cocaine choice and methamphetamine choice.

College age subjects learned & recalled a series of word lists prior to being injected with 0.2 or 0.3 mg/kg methamphetamine, 8 mg/kg scopolamine, or a placebo. Following injection, subjects were tested for their free recall & recognition of the words & they completed a short term digit recall task. Subjects who had previously received scopolamine were next injected with either 0.2 mg/kg or 0.3 mg/kg methamphetamine, physostigmine, or placebo, while other subjects received a placebo injection. The memory procedure was then repeated with a 2ND series of word lists. ... Scopolamine & methamphetamine did not affect recall of information learned prior to injection. Scopolamine did, however, impair performance in both the digit recall task & in the second series of memory tests. Physostigmine & methamphetamine alleviated most of the memory deficits & sedation produced by scopolamine. Methamphetamine impaired performance in both the digit recall task & in the 2ND series of memory tests. When given alone, it also produced subjective arousal & small improvement in recall of words learned after injection & large incr in incorrect responding.

Neurologic and circulatory reactions have been reported in patients who have received parenteral methamphetamine concomitantly with monoamine oxidase inhibitor drugs, and fatalities have occurred. Methamphetamine is therefore contraindicated during or within 14 days of administration of monoamine oxidase inhibitors.

Patients receiving concomitant therapy with tricyclic antidepressants and indirect-acting sympathomimetic amines (e.g., amphetamines) should be closely monitored, and dosage carefully adjusted.

For more Interactions (Complete) data for d-METHAMPHETAMINE (9 total), please visit the HSDB record page.

Using large amounts of these drugs can result in a condition known as amphetamine psychosis -- which can result in auditory, visual and tactile hallucinations, intense paranoia, irrational thoughts and beliefs, delusions, and mental confusion.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 900(SRC), determined from a structure estimation method(2), indicates that d-methamphetamine is expected to have low mobility in soil(SRC). The pKa of d-methamphetamine is 9.87(3), indicating that this compound will exist almost entirely in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization from moist soil is not expected because the compound exists as a cation and cations do not volatilize. d-Methamphetamine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.4X10-3 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation half-lives of 131 days in sandy loam and 502 days in loam(5) suggest that biodegradation in soil is dependent upon soil conditions(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 900(SRC), determined from a structure estimation method(2), indicates that d-methamphetamine is expected to adsorb to suspended solids and sediment(SRC). A pKa of 9.87(3) indicates d-methamphetamine will exist almost entirely in the cation form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), an estimated BCF of 11(SRC), from its log Kow of 2.07(5) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). d-Methamphetamine present at 1090 ng/L, decreased in concentration to 675 and 529 ng/L in duplicate test runs over 15 days using river microcosm bioreactors(6), suggesting that biodegradation may be an important environmental fate process in water(SRC). However d-methamphetamine is expected to undergo hydrolysis in the environment due to the presence of functional groups that hydrolyze under environmental conditions(7).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), d-methamphetamine, which has an estimated vapor pressure of 5.41X10-3 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase d-methamphetamine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 1 hour(SRC), calculated from its rate constant of 9.3X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). d-Methamphetamine does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

Individuals who use methamphetamine experience a rapid and intense onset of effects typically lasting 5 to 30 minutes, depending on the method of administration. Methamphetamine increases energy levels, suppresses appetite, and produces euphoria for a duration of 6 to 12 hours.

Methamphetamine is rapidly absorbed from the gastrointestinal tract with peak methamphetamine concentrations occurring in 3.13 to 6.3 hours post ingestion. Methamphetamine is also well absorbed following inhalation and following intranasal administration. 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.

IDENTIFICATION AND USE: Methamphetamine is a white solid odorless crystals. Indications: Narcolepsy and hyperkinetic states in children (as an adjunct to psychological, educational and social measures). Its misuse includes performance enhancement and relief of fatigue. It is a Schedule II Controlled Substance. HUMAN EXPOSURE AND TOXICITY: Main risks include: acute central nervous system (CNS) stimulation, cardiotoxicity causing tachycardia, arrhythmias, hypertension and cardiovascular collapse. High risk of dependency and abuse. Cardiovascular effects include: palpitation, chest pain, tachycardia, arrhythmias and hypertension; cardiovascular collapse can occur in severe poisoning. Myocardial ischemia, infarction and ventricular dysfunction are described. CNS effects include: stimulation of CNS, tremor, restlessness, agitation, insomnia, increased motor activity, headache, convulsions, coma and hyperreflexia. Stroke and cerebral vasculitis have been observed. Gastrointestinal effects include: vomiting, diarrhea and cramps. Acute transient ischemic colitis has occurred with chronic methamphetamine abuse. Genitourinary effects include: increased bladder sphincter tone which may cause dysuria, hesitancy and acute urinary retention. Renal failure can occur secondary to dehydration or rhabdomyolysis. Renal ischemia may be noted. Transient hyperthyroxinemia may be noted. Increased metabolic and muscular activity may result in hyperventilation and hyperthermia. Weight loss is common with chronic use. Hypo- and hyperkalemia have been reported. Dehydration is common. Fasciculations and rigidity may be noted. Rhabdomyolysis is an important consequence of severe amphetamine poisoning. Agitation, confusion, mood elevation, increased wakefulness, talkativeness, irritability and panic attacks are typical. Chronic abuse can cause delusions and paranoia. A withdrawal syndrome occurs after abrupt cessation following chronic use. 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. In fatal cases of poisoning in human patients, the panic state is followed by convulsions, coma and death from intracranial hemorrhages or cardiac arrhythmias. The use of amphetamine and its congeners for medical indications do not pose a significant risk to the fetus for congenital anomalies. They generally do not appear to be human teratogens. Mild withdrawal symptoms may be observed in the newborn, but the few studies of infant follow-up have not shown long-term sequelae. Illicit maternal use or abuse presents a significant risk to the fetus and newborn, including intrauterine growth retardation, premature delivery and the potential for increased maternal, fetal and neonatal morbidity. These poor outcomes are probably multifactorial in origin, involving multiple drug use, life-styles and poor maternal health. However, cerebral injuries occurring in newborns exposed in utero appear to be directly related to the vasoconstrictive properties of amphetamines. Sixty-five children were followed whose mothers were addicted during pregnancy, at least during the first trimester. Intelligence, psychological function, growth, and physical health were all within the normal range at eight years, but those children exposed throughout pregnancy tended to be more aggressive. ANIMAL STUDIES: The administration of high dose of methamphetamine causes long lasting damage to central dopaminergic and serotonergic neurons through a mechanism known to involve presynaptic, cytoplasmic stores of those transmitters dependent upon a free radical reaction in experimental animals. Confinement and aggregation markedly increased lethality of methamphetamine in mice. Pregnant sheep given methamphetamine appeared anxious, with quick side to side movements of the head and feet.

Methamphetamine use can lead to both physical and psychological dependence, accompanied by the development of tolerance. Because of the rapid development of tolerance, methamphetamine users frequently need to increase the dose to get to the satisfying "high," which can be very dangerous because the administration of too much methamphetamine also increases the risk of an overdose.

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.

Manifestations of acute overdosage with methamphetamine include restlessness, tremor, hyperreflexia, rapid respiration, confusion, assaultiveness, hallucinations, panic states, hyperpyrexia, and rhabdomyolysis. Fatigue and depression usually follow the central stimulation. Cardiovascular effects include arrhythmias, hypertension or hypotension, and circulatory collapse. Gastrointestinal symptoms include nausea, vomiting, diarrhea, and abdominal cramps. Fatal poisoning usually terminates in convulsions and coma.

d-Methamphetamine was present at an average loading rate of 806 and <18 g/day in influent and effluent, respectively, collected from a wastewater treatment plant in conjunction with a US major sporting event (National Football League's Super Bowl). Non-event loadings were 930 and <10 g/day(1). The compound was detected at a range of <0.1-0.3 ng/L, maximum concentration of 0.3 ng/L also reported, in unspecified UK surface water samples(2). The compound was detected at a mean concentration of 4.6 ng/L (range 0.8-8.4 ng/L; 14% samples positive) in influent sewage samples from the Ebro River Basin, Spain, sampled in October 2007 and July 2008. A median concentration of 1.3 ng/L (range 0.5-7.6 ng/L; 43% samples positive) was reported for effluent samples(3).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of d-methamphetamine can be estimated to be 900(SRC). According to a classification scheme(2), this estimated Koc value suggests that d-methamphetamine is expected to have low mobility in soil. The pKa of d-methamphetamine is 9.87(3), indicating that this compound will exist almost entirely in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

/SIGNS AND SYMPTOMS/ In fatal cases of poisoning in human patients, the panic state is followed by convulsions, coma and death from intracranial hemorrhages or cardiac arrythmias.

/SIGNS AND SYMPTOMS/ Injected intravenously, it induces intense euphoria (a "rush"). Overdoses may produce confusion, hallucinations, convulsions, mania, and acts of self-destruction. Its psychic and motor effects resemble those of cocaine but last longer.

/SIGNS AND SYMPTOMS/ Intravenous or smoked methamphetamine produces an abuse/dependence syndrome similar to that of cocaine.

/SIGNS AND SYMPTOMS/ Manifestations of acute overdosage with methamphetamine include restlessness, tremor, hyperreflexia, rapid respiration, confusion, assaultiveness, hallucinations, panic states, hyperpyrexia, and rhabdomyolysis. Fatigue and depression usually follow the central stimulation. Cardiovascular effects include arrhythmias, hypertension or hypotension, and circulatory collapse. Gastrointestinal symptoms include nausea, vomiting, diarrhea, and abdominal cramps. Fatal poisoning usually terminates in convulsions and coma.

For more Human Toxicity Excerpts (Complete) data for d-METHAMPHETAMINE (13 total), please visit the HSDB record page.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including methamphetamine hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Methamphetamine hydrochloride/

Schedule II shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... (d) Stimulants. Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation which contains any quantity of the following substances having a stimulant effect on the central nervous system: Methamphetamine, its salts, isomers, and salts of its isomers (DEA Code Number: 1105) is included on this list. /Methamphetamine, its salts, isomers, and salts of its isomers/

N - Nervous system

QN - Nervous system

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.

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.

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.

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.

44RAL3456C

METHAMPHETAMINE

Established Pharmacologic Class [EPC] - Amphetamine Anorectic

Chemical Structure [CS] - Amphetamines

Physiologic Effects [PE] - Appetite Suppression

Established Pharmacologic Class [EPC] - Central Nervous System Stimulant

A loosely defined group of drugs that tend to increase behavioral alertness, agitation, or excitation. They work by a variety of mechanisms, but usually not by direct excitation of neurons. The many drugs that have such actions as side effects to their main therapeutic use are not included here.

Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.

Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons.

Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters.

Drugs that block the transport of adrenergic transmitters into axon terminals or into storage vesicles within terminals. The tricyclic antidepressants (ANTIDEPRESSIVE AGENTS, TRICYCLIC) and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic transport. Many of these drugs also block transport of serotonin.

Drugs that block the transport of DOPAMINE into axon terminals or into storage vesicles within terminals. Most of the ADRENERGIC UPTAKE INHIBITORS also inhibit dopamine uptake.

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/

MEDICATION (VET)

MEDICATION

Methamphetamine, its salts, isomers, and salts of its isomers (DEA Code Number: 1105) are Schedule II controlled substances. /Methamphetamine, its salts, isomers, and salts of its isomers/

Schedule II Controlled Substance: (A) The drug or other substance has a high potential for abuse; (B) The drug or other substance has a currently accepted medical use in treatment in the United States or a currently accepted medical use with severe restrictions; and (C) Abuse of the drug or other substances may lead to severe psychological or physical dependence.

Adrenergic Agents; Adrenergic Uptake Inhibitors; Appetite Depressants; Central Nervous System Stimulants; Dopamine Agents; Dopamine Uptake Inhibitors; Sympathomimetics

For the treatment of Attention Deficit Disorder with Hyperactivity (ADHD) and exogenous obesity.

Can be prepared by reducing ephedrine or pseudoephedrine; ... Prepared by reducing the condensation product of benzyl methyl ketone and methylamine.

Prepared from phenylacetone and methylamine or from (-)-ephedrine.

Oral: tablets 5 mg, Desoxyn, C-II (Ovation)

Ice is a very pure form of methamphetamine hydrochloride (98-100%) ... /"Ice"/

Common street names: Batu, Bikers Coffee, Black Beauties, Chalk, Chicken Feed, Crank, Crystal, Glass, Go-Fast, Hiropon, Ice, Meth, Methlies Quick, Poor Man's Cocaine, Shabu, Shards, Speed, Stove Top, Tina, Trash, Tweak, Uppers, Ventana, Vidrio, Yaba, and Yellow Bam.

Methamphetamine (meth), a highly addictive drug, can be illegally manufactured using easily acquired chemicals; meth production can cause fires, explosions, injuries, and environmental contamination. To analyze injury incidence and trends, data on 1,325 meth-related chemical incidents reported to the Agency for Toxic Substances and Disease Registry's (ATSDR) Hazardous Substances Emergency Events Surveillance (HSEES) system and National Toxic Substance Incidents Program (NTSIP) by the five participating states (Louisiana, Oregon, Utah, New York, and Wisconsin) with complete information during 2001-2012 were examined. The findings suggested that meth-related chemical incidents increased with the drug's popularity (2001-2004), declined with legislation limiting access to precursor chemicals (2005-2007), and increased again as drug makers circumvented precursor restrictions (2008-2012). Seven percent of meth-related chemical incidents resulted in injuries to 162 persons, mostly members of the general public (97 persons, including 26 children) and law enforcement officials (42). Recent trends suggest a need for efforts to protect the general public, particularly children and law enforcement officials. Because individual state legislative actions can result in increased illegal meth production in neighboring states, a regional approach to prevention is recommended.

Illicit methamphetamine may be synthesized by a method that involves the reaction of lead acetate and phenylacetic acid to form phenyl-2-propanone, a precursor methamphetamine in the amalgam process.