ACT Amphetamine XR - 20MG
ACT Amphetamine XR - 20MG Uses, Dosage, Side Effects, Food Interaction and all others data.
Amphetamine, a compound discovered over 100 years ago, is one of the more restricted controlled drugs. It was previously used for a large variety of conditions and this changed until this point where its use is highly restricted. Amphetamine, with the chemical formula alpha-methylphenethylamine, was discovered in 1910 and first synthesized by 1927. After being proven to reduce drug-induced anesthesia and produce arousal and insomnia, amphetamine racemic mix was registered by Smith, Kline and French in 1935. Amphetamine structure presents one chiral center and it exists in the form of dextro- and levo-isomers. The first product of Smith, Kline and French was approved by the FDA on 1976.
During World War II, amphetamine was used to promote wakefulness in the soldiers. This use derived into a large overproduction of amphetamine and all the surplus after the war finalized ended up in the black market, producing the initiation of the illicit abuse.
From its mechanism of action, it has been demonstrated that amphetamine augments the concentration of noradrenaline in the prefrontal cortex and dopamine in the striatum on a dose and time-dependent manner. The indistinct release of neurotransmitters which include adrenaline is known to produce cardiovascular side effects.
Dextroamphetamine is the dextrorotary enantiomer of amphetamine. Dextroamphetamine was approved by the FDA in 2001 for the treatment of attention deficit hyperactivity disorder.
Dextroamphetamine is a noncatecholamine, sympathomimetic amine that acts as a CNS stimulant. Dextroamphetamine raises systolic and diastolic blood pressure, acts as a weak bronchodilator, and also acts as a respiratory stimulant. The general mechanism of action of dextroamphetamine has not been well established.
| Trade Name | ACT Amphetamine XR - 20MG |
| Generic | Amphetamine + dextroamphetamine |
| Type | Oral |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | United States |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Amphetamine is a CNS stimulant and sympathomimetic agent indicated for the treatment of Attention Deficit Hyperactivity Disorder (ADHD).
Amphetamine is indicated for the treatment of attention-deficit/hyperactivity disorders (ADHD) as well as for the treatment of central nervous system disorders such as narcolepsy.
ADHD is a complex disorder associated with the substantial heterogeneity in etiology, clinical presentation, and treatment outcome. ADHD comes from a complex interplay between interdependent genetic and non-genetic factors which cause complex mental disorders in children and teenagers.
On the other hand, narcolepsy is a chronic sleep disorder typically resenting during adolescence and characterized by excessive daytime sleepiness.
Amphetamine is also being used nowadays off-label for the treatment of obesity, depression and chronic pain.
Dextroamphetamine is a sympathomimetic agent used in the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy.
Dextroamphetamine is indicated for the treatment of attention deficit hyperactivity disorder (ADHD).
ACT Amphetamine XR - 20MG is also used to associated treatment for these conditions: Attention Deficit Hyperactivity Disorder (ADHD), BMI >30 kg/m2, Depression, Narcolepsy, Pain, ChronicAttention Deficit Hyperactivity Disorder (ADHD), Narcolepsy
How ACT Amphetamine XR - 20MG works
It is important to consider that amphetamine has a very similar structure to the catecholamine neurotransmitters mainly on the presence of a long planar conformation, the presence of an aromatic ring and nitrogen in the aryl side chain. Amphetamine, as well as other catecholamines, is taken into presynaptic nerve terminals by the association with two sodium ions and one chloride ion. The complex of the amphetamine with the ions is actively transported by monoamine reuptake transporters. As amphetamine acts competitively with the endogenous monoamines, the greater the number of amphetamines the more internalized amphetamine will be found.
Once inside the presynaptic terminal, amphetamine displaces other monoamines to be stored by VMAT2 which produces the pumping of the neurotransmitters into the synapse by a process called retro-transport. This process of release of neurotransmitters is approximately fourfold more potent in the d-isomer for the release of dopamine.
The mechanism of action of amphetamine is complemented by the inhibition of the reuptake and of monoamine oxidase which acts synergistically to produce a significant increase the monoamine concentration. This activity is not done as an inhibitor per se but more as a competitive substrate and thus, amphetamine is known to be a weak dopamine reuptake inhibitor, moderate noradrenaline reuptake inhibitor and very weak serotonin reuptake inhibitor. From this specific action, the l-isomer is known to be significantly less potent.
Lastly, amphetamine is known to be an inhibitor of the mitochondrial-bound enzyme MAO which is the catalytic enzyme in charge of degrading all the excess of neurotransmitters. This mechanism of action is often overpassed as amphetamine is a weak MAO inhibitor but this mechanism cannot be dismissed.
The exact mechanism of amphetamines as a class is not known. Dextroamphetamine acts by preventing reuptake, increasing release, and stimulating reverse-transport of dopamine in synaptic clefts in the striatum. Newer evidence shows amphetamines may also alter the number of dopamine transporters in synaptic clefts.
Toxicity
The mean lethal serum concentration is reported to be of 6.4 mg/l. Acute amphetamine overdose can lead to hyperthermia, respiratory depression, seizures, metabolic acidosis, renal failure, hepatic injury, and coma. Some of the neurologic effects have been shown to be agitation, aggressive behavior, irritability, headache, and hallucinations. In the cardiovascular site, there have been reports of arrhythmia, cardiomyopathy, myocardial infarction or ischemic stroke. Lastly, in the GI tract, there are reports if abdominal pain, vomiting, diarrhea, cramps, anorexia and GI hemorrhage. A dose of 1-2 g of amphetamine is known to cause severe intoxication but some chronic abusers can report usage of even 5-15 g per day.
In animal studies, there is no evidence of carcinogenic potential, not clastogenic or to affect fertility or early embryonic development.
Dextroamphetamine has been shown to be teratogenic and embryotoxic in mice at 41 times the maximum human dose. These effects were not seen in rat or rabbit studies, and the effects on human pregnancy have not been studied. The risk and benefit of use during pregnancy should be weighed as bone deformities, tracheoesophageal fistula, anal atresia, low birthweight, and withdrawl have been reported in the children of mothers who were taking dextroamphetamine during pregnancy. Mothers should not take amphetamines while nursing as the drug is excreted in breast milk. Long term effects of dextroamphetamine have not bee determined in pediatric patients and dextroamphetamine should be avoided in children under 3 years.
Volume of Distribution
Amphetamine is reported to have a high volume of distribution of 4 L/kg.
195L.
Elimination Route
Amphetamine is well absorbed in the gut and as it is a weak base hence the more basic the environment the more of the drug is found in a lipid-soluble form and the absorption through lipid-rich cell membranes is highly favored. The peak response of amphetamine occurs 1-3 hours after oral administration and approximately 15 minutes after injection and it presents a bioavailability of over 75%. Complete amphetamine absorption is usually done after 4-6 hours.
Bioavailability data of dextroamphetamine is not readily available, however there is no difference in bioavailability when taken with or without a meal.
Half Life
The half-life of amphetamine highly depends on the isomer. For d-amphetamine, the reported half-life is of approximately 9-11 hours while for l-amphetamine the half-life is reported to be of 11-14 hours. The urine pH can modify this pharmacokinetic parameter which can vary from 7 hours in acid urine to 34 hours for alkaline urine.
11.75 hours. In a study of post-stroke patients the half life was 16.0 hours in females and 12.4 hours in males. Studies in healthy populations show a half life of 7.9 hours.
Clearance
The reported normal clearance rate is of 0.7 L.h/kg. This clearance has been shown to get significantly reduced in patients with renal impairment reaching a value of 0.4 L.h/kg.
17L/h.
Elimination Route
The elimination of amphetamine is mainly via the urine from which about 40% of the excreted dose is found as unchanged amphetamine. About 90% of the administered amphetamine is eliminated 3 days after oral administration. The rate of elimination of amphetamine highly depends on the urine pH in which acidic pH will produce a higher excretion of amphetamine and basic pH produces a lower excretion.
A third of the drug is eliminated renally.
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