VYFOCIS 30

Indications

• Attention Deficit Hyperactivity Disorder (ADHD)
• Binge Eating Disorder (off-label usage)

Dosage

Children: For children aged 6 to 12 years, the starting dose is typically 30 mg once daily, which can be adjusted in increments of 10 to 20 mg weekly, with a maximum recommended dose of 70 mg per day. In children aged 13 years and older, the initial

Adults: The recommended starting dose for adults is 30 mg once daily, which may be increased in increments of 10 to 20 mg at weekly intervals, not exceeding a maximum dose of 70 mg per day.

Mechanism of action

Lisdexamfetamine is converted to dexamfetamine in the body. Dexamfetamine primarily acts by increasing the levels of norepinephrine and dopamine in the central nervous system through inhibition of their reuptake and stimulating their release. This results in enhanced attention and focus, decreased impulsivity, and reduced hyperactivity.

Pharmacodynamics

The pharmacodynamic effects of lisdexamfetamine include increased attention span, improved cognitive performance, and decreased impulsivity and hyperactivity in patients with ADHD. The onset of action is typically within 1 to 2 hours, with peak effects occurring about 3 to 4 hours after administration. The duration of action can last up to 12 hours, facilitating once-daily dosing.

Pharmacokinetics

Lisdexamfetamine is absorbed rapidly following oral administration, with peak plasma concentrations occurring approximately 3 to 5 hours after dosing. It is largely metabolized in the blood to dexamfetamine, which then exerts its therapeutic effects. The elimination half-life of dexamfetamine is approximately 10 to 13 hours. It is primarily excreted in the urine, with about 30% of the dose eliminated as unchanged drug. Factors such as age, weight, and renal function may influence pharmacokinetics.

Contra-indications

• Advanced arteriosclerosis
• Agitated states
• Hypertension (moderate to severe)
• Severe cardiovascular disease
• Susceptibility to angle-closure glaucoma
• Tics and Tourette syndrome
• Psychiatric disorders
• History of seizures

Adverse effects

• Abdominal pain
• Anxiety
• Decreased appetite
• Behaviour abnormality
• Constipation
• Diarrhoea
• Dizziness
• Dry mouth
• Dyspnoea
• Fatigue
• Feeling jittery
• Headache
• Hyperhidrosis
• Insomnia
• Mood altered
• Movement disorders
• Nausea
• Palpitations
• Sexual dysfunction
• Tachycardia
• Tremor
• Depression
• Visual disturbances
• Vomiting

Interactions

• Other amphetamines
• Drugs that may increase blood pressure or heart rate

Precautions

• Monitor growth in children
• Monitor for aggressive behaviour or hostility during initial therapy
• Avoid abrupt withdrawal
• Caution in patients with underlying cardiovascular conditions

Pregnancy

Use only if potential benefit outweighs risk.

Breast-feeding

Manufacturer advises to avoid, as the drug is present in breast milk.

Storage

Store in a cool, dry place away from direct sunlight.

Formulations

• Dexamfetamine sulfate 5 mg tablets
• Dexamfetamine sulfate 10 mg tablets
• Dexamfetamine sulfate oral solution (5 mg/5 ml)
• Dexamfetamine sulfate modified-release capsules

Indications

• Peripheral vascular disease
• Chronic venous insufficiency
• Raynaud's phenomenon
• Diabetic microangiopathy

Dosage

Children: Refer to the relevant pediatric dosing guidelines or clinical resources for appropriate dosing.

Adults: Refer to the specific product guidelines or clinical resources for adult dosing recommendations.

Mechanism of action

Dimesilate acts by inhibiting the synthesis of platelet-activating factor (PAF) and promoting the release of nitric oxide (NO) from endothelial cells. This results in vasodilation, increased blood flow, and improved oxygenation of tissues. The drug also has anti-inflammatory properties that contribute to its therapeutic effects in vascular conditions.

Pharmacodynamics

Dimesilate demonstrates a significant effect on microcirculation by reducing vascular resistance and increasing capillary permeability. This leads to improved tissue oxygenation and nutrient delivery, which is particularly beneficial in conditions characterized by poor blood flow. The anti-platelet and anti-inflammatory actions further enhance its effectiveness in treating circulatory disorders.

Pharmacokinetics

Dimesilate is absorbed rapidly following administration, with peak plasma concentrations occurring within a few hours. The drug is extensively metabolized in the liver, and its metabolites are excreted primarily via the kidneys. The half-life of dimesilate can vary, depending on individual patient factors such as age and liver function.

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Abdominal pain
• Dizziness
• Headache
• Rash

Precautions

• Use with caution in patients with renal impairment
• Monitor for signs of hypersensitivity
• Consider potential for additive effects with other medications affecting the gastrointestinal system

Pregnancy

Safety in pregnancy has not been established; use only if clearly needed and potential benefits outweigh risks.

Breast-feeding

Not recommended during breastfeeding due to insufficient data on excretion in human milk.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Formulations

• Oral tablets
• Injectable solution

Indications

• Attention-deficit hyperactivity disorder (ADHD)
• Binge eating disorder (BED)

Dosage

Children: For children aged 6 years and older, the recommended starting dose is usually

Adults: The recommended starting dose for adults with ADHD is typically 30 mg once daily in the morning, with potential adjustments based on clinical response and tolerability. The maximum recommended dose is 70 mg per day.

Mechanism of action

Lisdexamfetamine is converted to dextroamphetamine, which acts as a non-catecholamine sympathomimetic amine with central nervous system stimulant activity. Dextroamphetamine inhibits the dopamine transporter (DAT), noradrenaline transporter (NET), and vesicular monoamine transporter 2 (VMAT2), leading to increased availability of norepinephrine and dopamine in the extracellular space by blocking their reuptake into presynaptic neurons. This mechanism contributes to its efficacy in managing symptoms of ADHD and BED.

Pharmacodynamics

Upon administration, lisdexamfetamine is metabolized into dextroamphetamine, which penetrates the central nervous system. Dextroamphetamine enhances the release of norepinephrine and dopamine, resulting in increased neurotransmitter levels in the brain. This action is essential for improving attention and reducing impulsivity and hyperactivity in patients with ADHD, as well as curbing binge eating episodes in patients with BED.

Pharmacokinetics

Lisdexamfetamine is absorbed rapidly following oral administration and is converted to dextroamphetamine primarily in the blood. The peak plasma concentrations of dextroamphetamine occur approximately 1 to 2 hours after administration. The elimination half-life of dextroamphetamine is around 10 to 13 hours. The drug is primarily eliminated via the kidneys, with a significant portion excreted as unchanged drug.

Contra-indications

• Hypersensitivity to lisdexamfetamine or any of its components
• Severe cardiovascular disorders
• Hyperthyroidism
• Glaucoma
• History of drug abuse
• Concurrent use of monoamine oxidase inhibitors (MAOIs)

Adverse effects

• Insomnia
• Decreased appetite
• Dry mouth
• Headache
• Nausea
• Vomiting
• Irritability
• Increased heart rate
• Hypertension
• Anxiety

Interactions

• Monoamine oxidase inhibitors (MAOIs) - risk of hypertensive crisis
• Antihypertensives - may reduce efficacy
• Tricyclic antidepressants - increased risk of side effects
• Serotonergic agents - potential for serotonin syndrome

Precautions

• Monitor blood pressure and heart rate regularly
• Use with caution in patients with a history of substance use disorder
• Consider cardiovascular evaluation before starting treatment in patients with pre-existing heart conditions
• Assess for potential exacerbation of psychiatric symptoms

Pregnancy

Lisdexamfetamine is classified as category C. There is no adequate and well-controlled studies in pregnant women. The potential benefits must be weighed against the risks.

Breast-feeding

It is not known whether lisdexamfetamine is excreted in human milk. Caution should be exercised when administered to a nursing mother.

Storage

Store below 25 degrees Celsius in a tightly closed container. Protect from moisture and light.

Formulations

• Capsules: 30 mg, 50 mg, 70 mg

Mechanism of action

Lisdexamfetamine is a prodrug of dextroamphetamine, which is a noncatecholamine sympathomimetic amine with CNS stimulant activity. Dextroamphetamine is a known inhibitor of the dopamine transporter (DAT), noradrenaline transporter (NET) and vesicular monoamine transporter 2 (VMAT2), with a weaker affinity for the serotonin transporter (SERT). It is also a weak monoamine oxidase (MAO) inhibitor. Dextroamphetamine ultimately blocks the reuptake of norepinephrine and dopamine into the presynaptic neuron and increases catecholamine availability in the extracellular space. The exact mode of therapeutic action of lisdexamfetamine in ADHD and BED has not been fully elucidated; however, the clinical effects of lisdexamfetamine are believed to be linked to the pharmacological actions of dextroamphetamine. Lisdexamfetamine is a prodrug of dextroamphetamine. Amphetamines are non-catecholamine sympathomimetic amines with CNS stimulant activity. Amphetamines block the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. The parent drug, lisdexamfetamine, does not bind to the sites responsible for the reuptake of norepinephrine and dopamine in vitro.

Pharmacodynamics

Once administered, lisdexamfetamine is converted to its active metabolite, dextroamphetamine, which is taken up by the brain. Dextroamphetamine blocks the reuptake of norepinephrine and dopamine into the presynaptic neuron and increases the release of these monoamines into the extraneuronal space. The parent drug, lisdexamfetamine, does not bind to the sites responsible for the reuptake of norepinephrine and dopamine in vitro.