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{{MedTemplate
{{MedTemplate
| generic          = Mixed amphetamine salts
| generic          = Mixed amphetamine salts
| brand            = Adderall, Adderall XR
| brand            = Adderall, Adderall XR, Mydayis
| structure        = Amphetamine-white.svg
| structure        = Amphetamine-white.svg
| classes             = Psychostimulant, Amphetamine
| classes           = Psychostimulant, Amphetamine, CNS stimulant
| mechanism        = Increased production and decreased reuptake of NE and DA
| mechanism        = TAAR1 agonism, VMAT2 substrate, DAT/NET reverse transport — net release of dopamine and norepinephrine
| uses              = Inattention, productivity,  
| uses              = ADHD, narcolepsy
| formula          = C<sub>9</sub>H<sub>13</sub>N
| formula          = C<sub>9</sub>H<sub>13</sub>N (parent amphetamine)
| routes            = Oral, primarily
| routes            = Oral
| onset            = rapid
| onset            = IR: 30–60 min; XR: 1–2 h to peak effect
| duration          = 8-14h
| duration          = IR 4–6 h; XR 10–12 h; Mydayis 14–16 h
| halflife          =  
| halflife          = D-amphetamine ~10 h; L-amphetamine ~13 h (adults)
| bioavailability  = Oral: ~90%
| bioavailability  = ~75–90% (oral)
| pregnancy        = Class C
| pregnancy        = Category C
| legal            = Schedule II Controlled Substance
| legal            = Schedule II
| intro            = Discovered initially in 1887 as a chemical by Lazăr Edeleanu, and then as a drug in the late 1920s. It was initially noted to have a chiral center and two enantiomers, levoamphetamine and dextroamphetamine, the latter of which being significantly more psychoactive.
| intro            = '''Mixed amphetamine salts (MAS)''' — marketed primarily as '''Adderall''' — is a 3:1 mixture of dextroamphetamine and levoamphetamine salts (dextroamphetamine sulfate, amphetamine sulfate, dextroamphetamine saccharate, and amphetamine aspartate). Amphetamine was first synthesized in 1887 by Lazăr Edeleanu, then developed as a medicine in the late 1920s. It has a chiral center and two enantiomers, levoamphetamine and dextroamphetamine; the latter is significantly more centrally psychoactive, while the levo enantiomer contributes more to peripheral noradrenergic effects. MAS is FDA-approved for attention-deficit hyperactivity disorder and narcolepsy. As a Schedule II controlled substance it carries substantial dependence and misuse potential, particularly in academic and occupational settings where it is frequently used off-label as a cognitive enhancer.
| pharmacokinetics  = Absorption: Excellent bioavailability by all knows routes of administration, sources report ">75%" and "~90%". Distribution: The volume of distribution of amphetamine is 4 L/kg, and its plasma protein binding is less than 20%. Metabolism: Amphetamine is oxidized to form 4-hydroxyamphetamine, alpha-hydroxyamphetamine, or norephedrine. Both norephedrine and 4-hydroxyamphetamine are active metabolites and are further metabolized to form 4-hydroxy-norephedrine. The deamination of alpha-hydroxyamphetamine leads to the formation of phenylacetone, which is then metabolized to benzoic acid, its glucuronide conjugate, and hippuric acid, the glycine conjugate. CYP2D6 is crucial in the metabolism of hydroxyamphetamine. Due to the genetic polymorphism of CYP2D6, variations in amphetamine metabolism may occur. Additionally, amphetamine inhibits monoamine oxidase (MAO), and both CYP1A2 and CYP3A4 contribute to its metabolism.[https://www.ncbi.nlm.nih.gov/sites/books/NBK507808/ cite] Elimination: Amphetamine is primarily excreted in the urine as metabolites, including alpha-hydroxy-amphetamine, with approximately 30% to 40% of the dose recovered as unchanged amphetamine. Due to its pKa of 9.9, the urinary elimination of amphetamine is influenced by urine pH and flow rates. An alkaline urine pH reduces ionization, which leads to decreased renal elimination. In contrast, acidic pH and increased urine flow rates enhance renal clearance, surpassing glomerular filtration rates (GFR), which suggests that active tubular secretion plays a significant role in excretion. The half-life of the D-enantiomer is 9 hours in children aged 6 to 12, whereas the L-enantiomer has a half-life of 11 hours. In adolescents aged 13 to 17, the D-enantiomer has a half-life of 11 hours, and the L-enantiomer ranges from 13 to 14 hours. In adults, the D-enantiomer has a half-life of 10 hours, whereas the L-enantiomer has a half-life of 13 hours.
| pharmacokinetics  = '''Absorption:''' Excellent oral bioavailability — sources report ">75%" to "~90%". Food does not significantly affect total absorption but can delay peak concentration. '''Distribution:''' Volume of distribution ~4 L/kg; plasma protein binding less than 20%. Crosses the blood–brain barrier and placenta. '''Metabolism:''' Amphetamine is oxidized to 4-hydroxyamphetamine, α-hydroxyamphetamine, or norephedrine. Norephedrine and 4-hydroxyamphetamine are active metabolites and are further metabolized to 4-hydroxy-norephedrine. Deamination of α-hydroxyamphetamine yields phenylacetone, which is metabolized to benzoic acid and conjugated to its glucuronide and hippuric acid. '''CYP2D6''' is crucial for amphetamine metabolism; genetic polymorphism causes significant inter-patient variability in clearance. Amphetamine itself inhibits monoamine oxidase (MAO), and both CYP1A2 and CYP3A4 contribute to its metabolism.<ref>https://www.ncbi.nlm.nih.gov/sites/books/NBK507808/</ref> '''Elimination:''' Primarily renal — ~30–40% recovered as unchanged amphetamine, the rest as metabolites. Due to its pK<sub>a</sub> of 9.9, urinary elimination is highly pH-dependent: alkaline urine reduces ionization and decreases renal clearance, while acidic urine and high flow rates accelerate clearance via active tubular secretion. '''Half-life:''' The D-enantiomer has a half-life of 9 hours in children (6–12 y), 11 hours in adolescents (13–17 y), and 10 hours in adults. The L-enantiomer is consistently longer-lived: 11 hours in children, 13–14 hours in adolescents, 13 hours in adults.
| pharmacodynamics  = REUPTAKE INHIBITION. EXCRETION!
| pharmacodynamics  = Amphetamine produces its effects through several converging mechanisms at monoaminergic terminals:
| indications      = Inattention, Fatigue
* '''Trace amine-associated receptor 1 (TAAR1) agonism''' — activates TAAR1 in monoaminergic neurons, triggering PKA/PKC signaling that phosphorylates the dopamine and norepinephrine transporters (DAT, NET), causing them to internalize and reverse direction.
| dosing            = Start Adderall XR 5 mg first thing in the morning. If insufficent, may take 10 mg the next day. Can increase 5 mg daily up to 30 mg or until effect.
* '''VMAT2 substrate''' — enters the presynaptic terminal, displaces dopamine and norepinephrine from vesicles into the cytoplasm.
| effects          = so many
* '''Reverse transport via DAT/NET''' — the elevated cytoplasmic monoamine pool is then ejected into the synaptic cleft via the now-reversed transporters. '''This is the primary mechanism of action — release, not reuptake inhibition.'''
| adverse          = so few
* '''Weak reuptake inhibition''' at DAT and NET (secondary to release).
| contraindications = few
* '''MAO inhibition''' at higher concentrations, slowing presynaptic catabolism of monoamines.
| interactions      =  
* '''Serotonergic effects''' at high or supratherapeutic doses (relevant to overdose and serotonin syndrome risk).
| pregnancy_details =  
 
| monitoring        =  
The net result is a robust increase in synaptic dopamine and norepinephrine in prefrontal cortex, striatum, and nucleus accumbens — underlying both therapeutic (attention, executive function, wakefulness) and reinforcing (euphoria, abuse liability) effects.
| counseling        =  
| indications      = * Attention-deficit hyperactivity disorder (ADHD) in children, adolescents, and adults
* Narcolepsy
* Off-label: treatment-resistant depression (augmentation), excessive daytime sleepiness in shift-work disorder, cognitive symptoms in chronic illness
| dosing            = '''Adderall XR (adults, ADHD):''' Start 5–10 mg first thing in the morning. Titrate by 5 mg every 4–7 days as tolerated, up to 30 mg/day (FDA labeling). Some clinicians titrate further; doses >40 mg/day are off-label.
'''Adderall XR (children 6–12, ADHD):''' Start 5–10 mg AM; max 30 mg/day.
'''Adderall IR:''' Start 5 mg once or twice daily; titrate by 5 mg/week; max 40 mg/day in 2–3 divided doses.
'''Mydayis (long-acting, ≥13 y):''' 12.5 mg AM; max 25 mg/day (adults), 12.5 mg/day (adolescents).
'''Narcolepsy:''' 5–60 mg/day in divided doses.
'''Renal/hepatic impairment:''' caution; reduce dose. Avoid in severe renal impairment.
| effects          = ''Therapeutic:'' improved attention and executive function, reduced impulsivity and hyperactivity, increased wakefulness, mild euphoria, increased motivation, mild appetite suppression.
''Common adverse:'' decreased appetite (often dose-limiting), insomnia, dry mouth, irritability, anxiety, mild elevation of heart rate and blood pressure, headache, jaw clenching/bruxism, mild weight loss.
| adverse          = * '''Cardiovascular:''' tachycardia, hypertension, palpitations; rare but reported cases of sudden cardiac death in patients with structural heart disease (FDA warning)
* '''Psychiatric:''' anxiety, agitation, insomnia, irritability; rarely psychosis or mania (especially in patients with bipolar predisposition)
* '''Dependence and misuse''' — Schedule II controlled substance; high abuse liability, particularly when crushed/insufflated/injected
* '''Tolerance''' to therapeutic effects can develop with chronic high-dose use
* '''Growth suppression''' in children — modest reduction in height/weight velocity with chronic stimulant use
* '''Serotonin syndrome''' — especially in combination with serotonergic agents or MAOIs
* '''Stereotyped behaviors''' (skin-picking, repetitive movements) at higher doses
* '''Bruxism and TMJ symptoms'''
* '''Peripheral vasculopathy''' — Raynaud-like phenomenon, rare digital ischemia
* '''Lowered seizure threshold''' (caution in epilepsy)
* '''Hyperthermia''' — risk in hot environments or with vigorous exercise
* '''Withdrawal''' on abrupt discontinuation — fatigue, depression, hypersomnia, increased appetite ("crash")
| contraindications = * Hypersensitivity to amphetamines
* Concurrent MAOI use, or within 14 days of MAOI discontinuation
* Symptomatic cardiovascular disease, advanced atherosclerosis, moderate–severe hypertension
* Hyperthyroidism
* Glaucoma
* Agitated states
* History of substance use disorder (relative contraindication; careful risk-benefit)
* Caution: structural cardiac abnormalities, bipolar disorder, psychotic disorders, Tourette syndrome / tic disorders
| interactions      = * '''MAOIs''' (phenelzine, tranylcypromine, selegiline, linezolid) — hypertensive crisis, serotonin syndrome; contraindicated
* '''Serotonergic agents''' (SSRIs, SNRIs, triptans, tramadol) — serotonin syndrome risk
* '''Tricyclic antidepressants''' — additive cardiovascular effects
* '''Acidifying agents''' (ammonium chloride, ascorbic acid in large doses, fruit juices) — increase urinary clearance, reduce efficacy
* '''Alkalinizing agents''' (sodium bicarbonate, acetazolamide, antacids) — decrease clearance, prolong/intensify effects
* '''CYP2D6 inhibitors''' (fluoxetine, paroxetine, bupropion) — elevated amphetamine levels
* '''Antihypertensives''' — may be antagonized by amphetamine's pressor effects
* '''Sympathomimetics''' (pseudoephedrine, phenylephrine) — additive cardiovascular effects
* '''Alcohol''' — may mask intoxication; cardiac risk
* '''Caffeine''' — additive stimulant effects, anxiety
| pregnancy_details = Category C. Crosses the placenta. Prenatal amphetamine exposure has been associated with low birth weight, premature delivery, and neonatal withdrawal (agitation, dysphoria, lassitude). Long-term neurodevelopmental outcomes from prescribed therapeutic exposure are less clear and likely modest, but illicit-dose exposure is associated with significant developmental impact. Decision should be individualized; many patients defer ADHD treatment during pregnancy. Excreted in breast milk in clinically significant amounts — breastfeeding generally discouraged.
| monitoring        = * Baseline: cardiovascular history, blood pressure, heart rate, weight/height, mental health history (especially for psychosis/bipolar/substance use risk)
* Consider ECG if cardiac risk factors present
* At each visit: blood pressure, heart rate, weight (and height in children), efficacy, side effects, signs of misuse or diversion
* Periodically reassess continued need; consider drug holidays in children to assess ongoing benefit and minimize growth effects
* Sleep quality (insomnia is dose-limiting)
| counseling        = * Take in the morning to minimize insomnia; avoid afternoon dosing.
* '''Do not crush, chew, or split Adderall XR or Mydayis capsules''' — disrupts the controlled-release mechanism. (Capsules may be opened and sprinkled on applesauce if needed.)
* Take with or without food; high-acid beverages (orange juice, vitamin C) may reduce absorption.
* Stay well-hydrated, especially in heat or during exercise.
* Eat regular meals despite appetite suppression.
* Do not combine with alcohol — masks effects of both, increases cardiac strain.
* Do not share or sell — federal Schedule II controlled substance; serious legal and clinical consequences.
* Report chest pain, palpitations, severe agitation, hallucinations, or signs of poor circulation in extremities.
* Sudden discontinuation can cause a fatigue/depression "crash" — taper or plan for it.
| anecdotes        =  
| anecdotes        =  
| seealso          =  
| seealso          = [[Dextroamphetamine]], [[Lisdexamfetamine]], [[Methylphenidate]], [[Dexmethylphenidate]], [[Modafinil]], [[Atomoxetine]], [[Methamphetamine]]
| references        =  
| references        =  
}}
}}
Excellent bioavailability by all knows routes of administration, sources report ">75%" and "~90%".
'''Distribution:'''
The volume of distribution of amphetamine is 4 L/kg, and its plasma protein binding is less than 20%.
'''Metabolism:'''
Amphetamine is oxidized to form 4-hydroxyamphetamine, alpha-hydroxyamphetamine, or norephedrine. Both norephedrine and 4-hydroxyamphetamine are active metabolites and are further metabolized to form 4-hydroxy-norephedrine.
The deamination of alpha-hydroxyamphetamine leads to the formation of phenylacetone, which is then metabolized to benzoic acid, its glucuronide conjugate, and hippuric acid, the glycine conjugate.
'''CYP2D6''' is crucial in the metabolism of hydroxyamphetamine. Due to the genetic polymorphism of CYP2D6, variations in amphetamine metabolism may occur. Additionally, amphetamine inhibits monoamine oxidase (MAO), and both CYP1A2 and CYP3A4 contribute to its metabolism. [https://www.ncbi.nlm.nih.gov/sites/books/NBK507808/ cite]
'''Elimination:'''
Amphetamine is primarily excreted in the urine as metabolites, including alpha-hydroxy-amphetamine, with approximately 30% to 40% of the dose recovered as unchanged amphetamine. Due to its pKa of 9.9, the urinary elimination of amphetamine is influenced by urine pH and flow rates. An alkaline urine pH reduces ionization, which leads to decreased renal elimination. In contrast, acidic pH and increased urine flow rates enhance renal clearance, surpassing glomerular filtration rates (GFR), which suggests that active tubular secretion plays a significant role in excretion. The half-life of the D-enantiomer is 9 hours in children aged 6 to 12, whereas the L-enantiomer has a half-life of 11 hours. In adolescents aged 13 to 17, the D-enantiomer has a half-life of 11 hours, and the L-enantiomer ranges from 13 to 14 hours. In adults, the D-enantiomer has a half-life of 10 hours, whereas the L-enantiomer has a half-life of 13 hours.<h2 id="Pharmacodynamics">Pharmacodynamics</h2>
REUPTAKE INHIBITION. EXCRETION!<h2 id="Indications">Indications</h2>
Inattention, Fatigue<h2 id="Dosing">Dosing and titration</h2>
Start Adderall XR 5 mg first thing in the morning. If insufficent, may take 10 mg the next day. Can increase 5 mg daily up to 30 mg or until effect.<h2 id="Effects">Effects</h2>
so many<h2 id="Adverse">Adverse effects</h2>
so few<h2 id="Contraindications">Contraindications</h2><span></span>
few
[[Category:Medicines]]

Revision as of 08:10, 11 May 2026

Psychostimulant, Amphetamine, CNS stimulant
Mixed amphetamine salts
Adderall, Adderall XR, Mydayis
Mixed amphetamine salts (MAS) — marketed primarily as Adderall — is a 3:1 mixture of dextroamphetamine and levoamphetamine salts (dextroamphetamine sulfate, amphetamine sulfate, dextroamphetamine saccharate, and amphetamine aspartate). Amphetamine was first synthesized in 1887 by Lazăr Edeleanu, then developed as a medicine in the late 1920s. It has a chiral center and two enantiomers, levoamphetamine and dextroamphetamine; the latter is significantly more centrally psychoactive, while the levo enantiomer contributes more to peripheral noradrenergic effects. MAS is FDA-approved for attention-deficit hyperactivity disorder and narcolepsy. As a Schedule II controlled substance it carries substantial dependence and misuse potential, particularly in academic and occupational settings where it is frequently used off-label as a cognitive enhancer.

Experience

👥 2 personal reports · avg efficacy 90.0/100 · avg side-effect burden 30.0/100 · median use 8 months · median dose 17.5 mg/day · 100% still taking it
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Problems

  • Attention-deficit hyperactivity disorder (ADHD) in children, adolescents, and adults
  • Narcolepsy
  • Off-label: treatment-resistant depression (augmentation), excessive daytime sleepiness in shift-work disorder, cognitive symptoms in chronic illness
+ Add a problem

Titration strategies

Adderall XR (adults, ADHD): Start 5–10 mg first thing in the morning. Titrate by 5 mg every 4–7 days as tolerated, up to 30 mg/day (FDA labeling). Some clinicians titrate further; doses >40 mg/day are off-label. Adderall XR (children 6–12, ADHD): Start 5–10 mg AM; max 30 mg/day. Adderall IR: Start 5 mg once or twice daily; titrate by 5 mg/week; max 40 mg/day in 2–3 divided doses. Mydayis (long-acting, ≥13 y): 12.5 mg AM; max 25 mg/day (adults), 12.5 mg/day (adolescents). Narcolepsy: 5–60 mg/day in divided doses. Renal/hepatic impairment: caution; reduce dose. Avoid in severe renal impairment.

+ Add a titration strategy

Effects

Therapeutic: improved attention and executive function, reduced impulsivity and hyperactivity, increased wakefulness, mild euphoria, increased motivation, mild appetite suppression. Common adverse: decreased appetite (often dose-limiting), insomnia, dry mouth, irritability, anxiety, mild elevation of heart rate and blood pressure, headache, jaw clenching/bruxism, mild weight loss.

  • Cardiovascular: tachycardia, hypertension, palpitations; rare but reported cases of sudden cardiac death in patients with structural heart disease (FDA warning)
  • Psychiatric: anxiety, agitation, insomnia, irritability; rarely psychosis or mania (especially in patients with bipolar predisposition)
  • Dependence and misuse — Schedule II controlled substance; high abuse liability, particularly when crushed/insufflated/injected
  • Tolerance to therapeutic effects can develop with chronic high-dose use
  • Growth suppression in children — modest reduction in height/weight velocity with chronic stimulant use
  • Serotonin syndrome — especially in combination with serotonergic agents or MAOIs
  • Stereotyped behaviors (skin-picking, repetitive movements) at higher doses
  • Bruxism and TMJ symptoms
  • Peripheral vasculopathy — Raynaud-like phenomenon, rare digital ischemia
  • Lowered seizure threshold (caution in epilepsy)
  • Hyperthermia — risk in hot environments or with vigorous exercise
  • Withdrawal on abrupt discontinuation — fatigue, depression, hypersomnia, increased appetite ("crash")

+ Add an effect

Pharmacokinetics

Absorption: Excellent oral bioavailability — sources report ">75%" to "~90%". Food does not significantly affect total absorption but can delay peak concentration. Distribution: Volume of distribution ~4 L/kg; plasma protein binding less than 20%. Crosses the blood–brain barrier and placenta. Metabolism: Amphetamine is oxidized to 4-hydroxyamphetamine, α-hydroxyamphetamine, or norephedrine. Norephedrine and 4-hydroxyamphetamine are active metabolites and are further metabolized to 4-hydroxy-norephedrine. Deamination of α-hydroxyamphetamine yields phenylacetone, which is metabolized to benzoic acid and conjugated to its glucuronide and hippuric acid. CYP2D6 is crucial for amphetamine metabolism; genetic polymorphism causes significant inter-patient variability in clearance. Amphetamine itself inhibits monoamine oxidase (MAO), and both CYP1A2 and CYP3A4 contribute to its metabolism.[1] Elimination: Primarily renal — ~30–40% recovered as unchanged amphetamine, the rest as metabolites. Due to its pKa of 9.9, urinary elimination is highly pH-dependent: alkaline urine reduces ionization and decreases renal clearance, while acidic urine and high flow rates accelerate clearance via active tubular secretion. Half-life: The D-enantiomer has a half-life of 9 hours in children (6–12 y), 11 hours in adolescents (13–17 y), and 10 hours in adults. The L-enantiomer is consistently longer-lived: 11 hours in children, 13–14 hours in adolescents, 13 hours in adults.

Pharmacodynamics

Amphetamine produces its effects through several converging mechanisms at monoaminergic terminals:

  • Trace amine-associated receptor 1 (TAAR1) agonism — activates TAAR1 in monoaminergic neurons, triggering PKA/PKC signaling that phosphorylates the dopamine and norepinephrine transporters (DAT, NET), causing them to internalize and reverse direction.
  • VMAT2 substrate — enters the presynaptic terminal, displaces dopamine and norepinephrine from vesicles into the cytoplasm.
  • Reverse transport via DAT/NET — the elevated cytoplasmic monoamine pool is then ejected into the synaptic cleft via the now-reversed transporters. This is the primary mechanism of action — release, not reuptake inhibition.
  • Weak reuptake inhibition at DAT and NET (secondary to release).
  • MAO inhibition at higher concentrations, slowing presynaptic catabolism of monoamines.
  • Serotonergic effects at high or supratherapeutic doses (relevant to overdose and serotonin syndrome risk).
The net result is a robust increase in synaptic dopamine and norepinephrine in prefrontal cortex, striatum, and nucleus accumbens — underlying both therapeutic (attention, executive function, wakefulness) and reinforcing (euphoria, abuse liability) effects.

Interactions

  • MAOIs (phenelzine, tranylcypromine, selegiline, linezolid) — hypertensive crisis, serotonin syndrome; contraindicated
  • Serotonergic agents (SSRIs, SNRIs, triptans, tramadol) — serotonin syndrome risk
  • Tricyclic antidepressants — additive cardiovascular effects
  • Acidifying agents (ammonium chloride, ascorbic acid in large doses, fruit juices) — increase urinary clearance, reduce efficacy
  • Alkalinizing agents (sodium bicarbonate, acetazolamide, antacids) — decrease clearance, prolong/intensify effects
  • CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) — elevated amphetamine levels
  • Antihypertensives — may be antagonized by amphetamine's pressor effects
  • Sympathomimetics (pseudoephedrine, phenylephrine) — additive cardiovascular effects
  • Alcohol — may mask intoxication; cardiac risk
  • Caffeine — additive stimulant effects, anxiety

    Pregnancy and lactation

Category C. Crosses the placenta. Prenatal amphetamine exposure has been associated with low birth weight, premature delivery, and neonatal withdrawal (agitation, dysphoria, lassitude). Long-term neurodevelopmental outcomes from prescribed therapeutic exposure are less clear and likely modest, but illicit-dose exposure is associated with significant developmental impact. Decision should be individualized; many patients defer ADHD treatment during pregnancy. Excreted in breast milk in clinically significant amounts — breastfeeding generally discouraged.

Monitoring

  • Baseline: cardiovascular history, blood pressure, heart rate, weight/height, mental health history (especially for psychosis/bipolar/substance use risk)
  • Consider ECG if cardiac risk factors present
  • At each visit: blood pressure, heart rate, weight (and height in children), efficacy, side effects, signs of misuse or diversion
  • Periodically reassess continued need; consider drug holidays in children to assess ongoing benefit and minimize growth effects
  • Sleep quality (insomnia is dose-limiting)

    Patient counseling

  • Take in the morning to minimize insomnia; avoid afternoon dosing.
  • Do not crush, chew, or split Adderall XR or Mydayis capsules — disrupts the controlled-release mechanism. (Capsules may be opened and sprinkled on applesauce if needed.)
  • Take with or without food; high-acid beverages (orange juice, vitamin C) may reduce absorption.
  • Stay well-hydrated, especially in heat or during exercise.
  • Eat regular meals despite appetite suppression.
  • Do not combine with alcohol — masks effects of both, increases cardiac strain.
  • Do not share or sell — federal Schedule II controlled substance; serious legal and clinical consequences.
  • Report chest pain, palpitations, severe agitation, hallucinations, or signs of poor circulation in extremities.
  • Sudden discontinuation can cause a fatigue/depression "crash" — taper or plan for it.

    Relevant anecdote

No anecdotes yet. Share a relevant one.

+ Add an anecdote

Relevant Literature

No literature entries yet.

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See also

Dextroamphetamine, Lisdexamfetamine, Methylphenidate, Dexmethylphenidate, Modafinil, Atomoxetine, Methamphetamine
Structure of Mixed amphetamine salts
Summary
Classes
Psychostimulant, Amphetamine, CNS stimulant
Common uses
+ 2 more uses →
Pharmacy
Pharmacology
Routes
Oral
Onset
IR: 30–60 min; XR: 1–2 h to peak effect
Duration
IR 4–6 h; XR 10–12 h; Mydayis 14–16 h
Half-life
D-amphetamine ~10 h; L-amphetamine ~13 h (adults)
Bioavailability
~75–90% (oral)
Pregnancy
Category C
Legal status
Schedule II
Purported mechanism
TAAR1 agonism, VMAT2 substrate, DAT/NET reverse transport — net release of dopamine and norepinephrine
  1. ↑ https://www.ncbi.nlm.nih.gov/sites/books/NBK507808/
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