Attenade
Attenade Uses, Dosage, Side Effects, Food Interaction and all others data.
Attenade is the dextrorotary form of methylphenidate introduced in 2002. It is a norepinephrine-dopamine reuptake inhibitor (NDRI) and thus a psychostimulant. It is used for treatment of Attention Deficit Hyperactivity Disorder (ADHD). The d-isomer is thought to have greater effect with fewer side effects than the l-isomer or the racemic mixture.
Attenade is the d-enantiomer of methylphenidate. This enantiomer is more pharmacologically active than the racemic mixture and may block norepinephrine and dopamine reuptake in synapses.
Trade Name | Attenade |
Availability | Prescription only |
Generic | Dexmethylphenidate |
Dexmethylphenidate Other Names | d-threo-methylphenidate, D-TMP, Dexmethylphenidate, Dexméthylphénidate, Dexmethylphenidatum, Dexmetilfenidato |
Related Drugs | Adderall, Vyvanse, methylphenidate, Concerta, Strattera, Ritalin |
Type | |
Formula | C14H19NO2 |
Weight | Average: 233.3062 Monoisotopic: 233.141578857 |
Protein binding | 12-15% of dexmethylphenidate is protein bound. However, other studies have observed 15.2±5.2% protein binding in children and 16.2±1.1% in adults. |
Groups | Approved, Investigational |
Therapeutic Class | |
Manufacturer | |
Available Country | |
Last Updated: | September 19, 2023 at 7:00 am |
Uses
Attenade is a norepinephrine-dopamine reuptake inhibitor used in the treatment of ADHD in conjunction with other therapies.
Attenade is used as a treatment for ADHD, ideally in conjunction with psychological, educational, behavioral or other forms of treatment.
Attenade is also used to associated treatment for these conditions: Attention Deficit Hyperactivity Disorder (ADHD)
How Attenade works
Methylphenidate inhibits dopamine and norepinephrine reuptake transporters in synapses, especially in the thalamus and striatum. One study shows no detectable difference in the caudal prefrontal cortex of treated or untreated monkeys, though multiple rat studies show activity on the prefrontal cortex. Imaging of human brains after administration of methylphenidate shows changes to blood flow of various regions of the brain including the striatum, supplementary motor area, and posterior parietal cortex.
Toxicity
There is no difference in effect across genders. The difference in effect across racial groups, patients under 6 years, renal impairment, hepatic impairment, pregnancy, lactation, and geriatric patients has not been well studied. Patients with renal impairment are not expected to need dose adjustment as the drug is not mainly cleared renally. Animal studies in pregnant and lactating rats showed delayed fetal skeletal ossification, and reduced weight gain in male offspring. Due to these studies, caution must be exercised and the benefits and risks of taking this drug must be weighed. It is unlikely that dexmethylphenidate is carcinogenic but B6C3F1 mice, which are sensitive to the development of hepatic tumours, developed hepatoblastomas at 2 times the maximum recommended human dose. Methylpheidate was not found to be mutagenic but is weakly clastogenic in Chinese Hamster Ovary cells. Methylphenidate does not impair fertility in animal studies.
Food Interaction
- Avoid alcohol. Alcohol inhibits the metabolism of dexmethylphenidate.
- Take with or without food.
Attenade Hypertension interaction
[Major] The use of CNS stimulants is contraindicated in patients with significant cardiovascular impairment such as uncompensated heart failure, severe coronary disease, severe hypertension (including that associated with hyperthyroidism or pheochromocytoma), cardiac structural abnormalities, serious arrhythmias, etc.
Sudden death has been reported in adults and children taking CNS stimulant treatment.
Additionally, stroke, myocardial infarction, chest pain, syncope, arrhythmias and other symptoms have been reported in adults under treatment.
A careful assessment of the cardiovascular status should be done in patients being considered for treatment.
This includes family history, physical exam and further cardiac evaluation (EKG and echocardiogram).
Patients who develop symptoms should have a detailed cardiac evaluation and if needed, treatment should be suspended.
Hypertension interaction[Major] CNS stimulant medications have shown to increase blood pressure, and their use might be contraindicated in patients with severe hypertension.
Caution should be used when administering to patients with preexisting high blood pressure and other cardiovascular conditions.
All patients under treatment should be regularly monitored for changes in blood pressure and heart rate.
Hypertension interaction[Major] Methylphenidate (racemic) and dexmethylphenidate (the more pharmacologically active d-enantiomer) exhibit sympathomimetic activity and may elevate blood pressure and pulse rate.
Therapy with these agents should be administered cautiously in patients with hypertension.
Blood pressure should be monitored periodically during therapy.
Attenade Drug Interaction
Moderate: escitalopram, escitalopram, fluoxetine, fluoxetine, sertraline, sertralineUnknown: aripiprazole, aripiprazole, amphetamine / dextroamphetamine, amphetamine / dextroamphetamine, methylphenidate, methylphenidate, pregabalin, pregabalin, atomoxetine, atomoxetine, cholecalciferol, cholecalciferol, lisdexamfetamine, lisdexamfetamine
Volume of Distribution
2.65L/kg when administered intravenously.
Elimination Route
Taking dexmethylphenidate with or without food does not affect patients in a clinically relevant way. 90% of an oral dose is absorbed but as a result of hepatic first pass metabolism, oral bioavailability of dexmethylphenidate is 23% compared to l-methylphenidate with an oral bioavailability of 5% . Maximum concentration is generally reached in 1-1.5 hours.
Half Life
The mean terminal half life is approximately 2.2 hours. However other studies have shown 3.8-3.9 hours, or 5.96 hours after intravenous administration and 5.69 hours following an oral dose.
Clearance
0.40L/hr/kg following an intravenous dose and a renal clearance of 0.005L/hr/kg.
Elimination Route
Attenade is mainly eliminated renally. After 48 hours, 90% of the dose is collected in the urine and 3.3% is collected from feces.
Innovators Monograph
You find simplified version here Attenade