Amsustain - General Information

Amsustain is the dextrorotary stereoisomer of the amphetamine molecule, which can take two different forms. It is a slightly polar, weak base and is lipophilic.


Pharmacology of Amsustain

Amphetamines such as dextroamphetamine are noncatecholamine, sympathomimetic amines with CNS stimulant activity. Peripheral actions include elevations of systolic and diastolic blood pressures and weak bronchodilator and respiratory stimulant action. There is neither specific evidence that clearly establishes the mechanism whereby amphetamines produce mental and behavioral effects in children, nor conclusive evidence regarding how these effects relate to the condition of the central nervous system.


Amsustain for patients

Amphetamines may impair the ability of the patient to engage in potentially hazardous activities such as operating machinery or vehicles; the patient should therefore be cautioned accordingly.


Amsustain Interactions

Acidifying agents: Gastrointestinal acidifying agents (guanethidine, reserpine, glutamic acid HCl, ascorbic acid, fruit juices, etc.) lower absorption of amphetamines. Urinary acidifying agents (ammonium chloride, sodium acid phosphate, etc.) increase the concentration of the ionized species of the amphetamine molecule, thereby increasing urinary excretion. Both groups of agents lower blood levels and efficacy of amphetamines.

Adrenergic blockers: Adrenergic blockers are inhibited by amphetamines.

Alkalinizing agents: Gastrointestinal alkalinizing agents (sodium bicarbonate, etc.) increase absorption of amphetamines. Urinary alkalinizing agents (acetazolamide, some thiazides) increase the concentration of the non-ionized species of the amphetamine molecule, thereby decreasing urinary excretion. Both groups of agents increase blood levels and therefore potentiate the actions of amphetamines.

Antidepressants, tricyclic: Amphetamines may enhance the activity of tricyclic or sympathomimetic agents; d-amphetamine with desipramine or protriptyline and possibly other tricyclics cause striking and sustained increases in the concentration of d-amphetamine in the brain; cardiovascular effects can be potentiated.

MAO inhibitors: MAOI antidepressants, as well as a metabolite of furazolidone, slow amphetamine metabolism. This slowing potentiates amphetamines, increasing their effect on the release of norepinephrine and other monoamines from adrenergic nerve endings; this can cause headaches and other signs of hypertensive crisis. A variety of neurological toxic effects and malignant hyperpyrexia can occur, sometimes with fatal results.

Antihistamines: Amphetamines may counteract the sedative effect of antihistamines.

Antihypertensives: Amphetamines may antagonize the hypotensive effects of antihypertensives.

Chlorpromazine: Chlorpromazine blocks dopamine and norepinephrine reuptake, thus inhibiting the central stimulant effects of amphetamines, and can be used to treat amphetamine poisoning.

Ethosuximide: Amphetamines may delay intestinal absorption of ethosuximide.

Haloperidol: Haloperidol blocks dopamine and norepinephrine reuptake, thus inhibiting the central stimulant effects of amphetamines.

Lithium carbonate: The stimulatory effects of amphetamines may be inhibited by lithium carbonate.

Meperidine: Amphetamines potentiate the analgesic effect of meperidine.

Methenamine therapy: Urinary excretion of amphetamines is increased, and efficacy is reduced, by acidifying agents used in methenamine therapy.

Norepinephrine: Amphetamines enhance the adrenergic effect of norepinephrine.

Phenobarbital: Amphetamines may delay intestinal absorption of phenobarbital; co-administration of phenobarbital may produce a synergistic anticonvulsant action.

Phenytoin: Amphetamines may delay intestinal absorption of phenytoin; co-administration of phenytoin may produce a synergistic anticonvulsant action.

Propoxyphene: In cases of propoxyphene overdosage, amphetamine CNS stimulation is potentiated and fatal convulsions can occur.

Veratrum alkaloids: Amphetamines inhibit the hypotensive effect of veratrum alkaloids.

Drug/Laboratory Test Interactions: Amphetamines can cause a significant elevation in plasma corticosteroid levels. This increase is greatest in the evening.

Amphetamines may interfere with urinary steroid determinations.


Amsustain Contraindications

Advanced arteriosclerosis, symptomatic cardiovascular disease, moderate to severe hypertension, hyperthyroidism, known hypersensitivity or idiosyncrasy to the sympathomimetic amines, glaucoma.

Agitated states.

Patients with a history of drug abuse.

During or within 14 days following the administration of monoamine oxidase inhibitors (hypertensive crises may result).


Additional information about Amsustain

Amsustain Indication: Used to treat attention deficit hyperactivity disorder (ADHD).
Mechanism Of Action: The exact mechanism of action is not known. Amsustain stimulates the release of norepinephrine from central adrenergic receptors. At higher dosages, it causes release of dopamine from the mesocorticolimbic system and the nigrostriatal dopamine systems. Amsustain may also act as a direct agonist on central 5-HT receptors and may inhibit monoamine oxidase (MAO). In the periphery, amphetamines are believed to cause the release of noradrenaline by acting on the adrenergic nerve terminals and alpha- and beta-receptors. Modulation of serotonergic pathways may contribute to the calming affect.
Drug Interactions: Not Available
Food Interactions: Not Available
Generic Name: Dextroamphetamine
Synonyms: S(+)-amphetamine; Dextroamphetamine; Dexanfetamina [inn-spanish]; Dexamphetaminum [inn-latin]; Dexamfetaminum [inn-latin]; Dexamfetamine; Dexamfetamina [inn-spanish]; Desamfetamina; D-amphetamine; D-am; D-alpha-methylphenethylamine; D-2-Amino-1-phenylpropane; D-1-Phenyl-2-aminopropane; d-1-Phenyl-2-aminopropan [German]; D-1-Phenyl-2-aminopropan; D-(s)-amphetamine; D-(+)-amphetamine; 1-Methyl-2-phenylethylamine; (s)-amphetamine; (s)-alpha-phenylethylamine; (s)-alpha-methylphenethylamine; (s)-alpha-methylbenzeneethanamine; (S)-1-phenyl-2-propylamine; (S)-1-Phenyl-2-propanamine; (S)-1-phenyl-2-aminopropane; (s)-(+)-beta-phenylisopropylamine; (s)-(+)-amphetamine; (2S)-1-phenylpropan-2-amine; (2S)-(+)-Amphetamine; (+)-phenaminum; (+)-amphetamine; (+)-alpha-methylphenylethylamine; (+)-alpha-methylphenethylamine; (+)-(s)-amphetamine; Dexamphetamine; Dextroamphetamine sulfate
Drug Category: Adrenergic Agents; Adrenergic Uptake Inhibitors; Central Nervous System Stimulants; Dopamine Agents; Dopamine Uptake Inhibitors; Sympathomimetics
Drug Type: Small Molecule; Illicit; Approved

Other Brand Names containing Dextroamphetamine: Amsustain; Dephadren; Desoxyn; Dexacaps; Dexadrine; Dexedrine; Dexedrine Spansule; Dexidrine; Sympamin; Dextrostat;
Absorption: Oral bioavailability is over 75%.
Toxicity (Overdose): In rats, the oral LD50 of dextroamphetamine sulfate is 96.8 mg/kg. Manifestations of acute overdosage with amphetamines include restlessness, tremor, hyperreflexia, rhabdomyolysis, rapid respiration, hyperpyrexia, confusion, assaultiveness, hallucinations, panic states. 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 is usually preceded by convulsions and coma.
Protein Binding: Not Available
Biotransformation: Hepatic.
Half Life: 10–28 hours (average is approximately 12 hours)
Dosage Forms of Amsustain: Tablet Oral
Capsule, extended release Oral
Chemical IUPAC Name: (2S)-1-phenylpropan-2-amine
Chemical Formula: C9H13N
Dextroamphetamine on Wikipedia:
Organisms Affected: Humans and other mammals