Mixed amphetamine salts - Revision history

MDElliottMD: Em-dash sweep: replace em-dash with comma per project rule; PendellsCorner verbatim quotes preserved.

2026-05-19T03:16:09Z

Em-dash sweep: replace em-dash with comma per project rule; PendellsCorner verbatim quotes preserved.

MDElliottMD: Recategorize: Stimulants -> Psychostimulants

2026-05-17T10:50:54Z

Recategorize: Stimulants -> Psychostimulants

← Older revision		Revision as of 10:50, 17 May 2026
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	}}		}}

	[[Category:~~Stimulants~~]]		[[Category:Psychostimulants]]
	[[Category:Amphetamines]]		[[Category:Amphetamines]]

MDElliottMD: Recategorize: Stimulants & Wake-Promoting Agents -> Stimulants

2026-05-17T10:45:09Z

Recategorize: Stimulants & Wake-Promoting Agents -> Stimulants

← Older revision		Revision as of 10:45, 17 May 2026
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	}}		}}

	[[Category:Stimulants ~~& Wake-Promoting Agents~~]]		[[Category:Stimulants]]
	[[Category:Amphetamines]]		[[Category:Amphetamines]]

MDElliottMD: Migrate tags to (Phase 2 of indications-to-problems rebuild)

2026-05-17T00:11:52Z

Migrate <indication> tags to <problem> (Phase 2 of indications-to-problems rebuild)

← Older revision		Revision as of 00:11, 17 May 2026
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	\| 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).		\| 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 med in the late 1920s. "Adderall" was approved by the FDA in 1996, and has since become one of the most popular meds in the United States. Adderall/MAS is FDA-approved for attention-deficit hyperactivity disorder and narcolepsy. It is listed in Schedule II of the Controlled Substances Act, and so is tightly regulated in the United States as well as many other countries around the world.		Amphetamine was first synthesized in 1887 by Lazăr Edeleanu, then developed as a med in the late 1920s. "Adderall" was approved by the FDA in 1996, and has since become one of the most popular meds in the United States. Adderall/MAS is FDA-approved for attention-deficit hyperactivity disorder and narcolepsy. It is listed in Schedule II of the Controlled Substances Act, and so is tightly regulated in the United States as well as many other countries around the world.
	\| indications = <~~indication~~ ref="adhd" author="MDElliottMD"/>		\| indications = <problem ref="adhd" author="MDElliottMD"/>
	<~~indication~~ ref="narcolepsy" author="MDElliottMD"/>		<problem ref="narcolepsy" author="MDElliottMD"/>
	<~~indication~~ ref="trd-augment" author="MDElliottMD">		<problem ref="trd-augment" author="MDElliottMD">
	Off-label.		Off-label.
	</~~indication~~>		</problem>
	<~~indication~~ ref="shift-work" author="MDElliottMD">		<problem ref="shift-work" author="MDElliottMD">
	Off-label.		Off-label.
	</~~indication~~>		</problem>
	<~~indication~~ ref="chronic-illness-cog" author="MDElliottMD">		<problem ref="chronic-illness-cog" author="MDElliottMD">
	Off-label.		Off-label.
	</~~indication~~>		</problem>

	<~~indication~~ ref="impulsivity" author="MDElliottMD"/>		<problem ref="impulsivity" author="MDElliottMD"/>

	<~~indication~~ ref="distractibility" author="MDElliottMD">		<problem ref="distractibility" author="MDElliottMD">
	Impoved sustained attention by decreasing distractibility		Impoved sustained attention by decreasing distractibility
	</~~indication~~>		</problem>
	\| dosing = <titration slug="typical-adult" title="Typical Adult" author="MDElliottMD">		\| dosing = <titration slug="typical-adult" title="Typical Adult" author="MDElliottMD">
	Start at 5 mg XR; may increase by 5 mg each day until the desired effect is reached, up to 30 mg XR to start, and up to 60 mg XR eventually if necessary, in 10 mg increments.		Start at 5 mg XR; may increase by 5 mg each day until the desired effect is reached, up to 30 mg XR to start, and up to 60 mg XR eventually if necessary, in 10 mg increments.

Maintenance script: Terminology: medicine → med (shorter form per user preference)

2026-05-16T02:42:46Z

Terminology: medicine → med (shorter form per user preference)

← Older revision		Revision as of 02:42, 16 May 2026
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	\| mechanism = TAAR1 agonism, VMAT2 substrate, DAT/NET reverse transport — net release of dopamine and norepinephrine		\| mechanism = TAAR1 agonism, VMAT2 substrate, DAT/NET reverse transport — net release of dopamine and norepinephrine
	\| 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).		\| 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. "Adderall" was approved by the FDA in 1996, and has since become one of the most popular ~~medicines~~ in the United States. Adderall/MAS is FDA-approved for attention-deficit hyperactivity disorder and narcolepsy. It is listed in Schedule II of the Controlled Substances Act, and so is tightly regulated in the United States as well as many other countries around the world.		Amphetamine was first synthesized in 1887 by Lazăr Edeleanu, then developed as a med in the late 1920s. "Adderall" was approved by the FDA in 1996, and has since become one of the most popular meds in the United States. Adderall/MAS is FDA-approved for attention-deficit hyperactivity disorder and narcolepsy. It is listed in Schedule II of the Controlled Substances Act, and so is tightly regulated in the United States as well as many other countries around the world.
	\| indications = <indication ref="adhd" author="MDElliottMD"/>		\| indications = <indication ref="adhd" author="MDElliottMD"/>
	<indication ref="narcolepsy" author="MDElliottMD"/>		<indication ref="narcolepsy" author="MDElliottMD"/>
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	\| monitoring = * Baseline: cardiovascular history, weight/height, mental health history (especially for psychosis/bipolar/substance use risk), (optional) blood pressure, (optional) heart rate,		\| monitoring = * Baseline: cardiovascular history, weight/height, mental health history (especially for psychosis/bipolar/substance use risk), (optional) blood pressure, (optional) heart rate,
	* At each visit: efficacy, side effects, general well-being		* At each visit: efficacy, side effects, general well-being
	* Periodically reassess continued need; consider ~~medicine~~ holidays to assess ongoing benefit		* Periodically reassess continued need; consider med holidays to assess ongoing benefit
	* Sleep quality (insomnia is dose-limiting)		* Sleep quality (insomnia is dose-limiting)
	\| counseling = * Take first thing in the morning to minimize insomnia; avoid (late) afternoon dosing.		\| counseling = * Take first thing in the morning to minimize insomnia; avoid (late) afternoon dosing.

Maintenance script: Terminology sweep (site-wide): drug/medication → medicine

2026-05-16T02:30:55Z

Terminology sweep (site-wide): drug/medication → medicine

Savijuana: Pharmacopedia: approved experience contribution

2026-05-15T06:07:25Z

Pharmacopedia: approved experience contribution

← Older revision		Revision as of 06:07, 15 May 2026
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	* <effect ref="withdrawal" author="MDElliottMD">Low motivation, low mood, hypersomnia, increased appetite on abrupt discontinuation.</effect>		* <effect ref="withdrawal" author="MDElliottMD">Low motivation, low mood, hypersomnia, increased appetite on abrupt discontinuation.</effect>
	* <effect ref="urinary-retention" author="MDElliottMD">Difficult/slow urination</effect>		* <effect ref="urinary-retention" author="MDElliottMD">Difficult/slow urination</effect>

			<effect ref="focus-intensification"/>

			<effect ref="appetite-suppression"/>

			<effect ref="alertness"/>

			<effect ref="executive-functioning"/>
	\| pk_absorption = Excellent oral bioavailability — sources report ">75%" to "~90%". Food does not significantly affect total absorption but can delay peak concentration.		\| pk_absorption = Excellent oral bioavailability — sources report ">75%" to "~90%". Food does not significantly affect total absorption but can delay peak concentration.
	\| pk_distribution = Volume of distribution ~4 L/kg; plasma protein binding less than 20%. Crosses the blood–brain barrier and placenta.		\| pk_distribution = Volume of distribution ~4 L/kg; plasma protein binding less than 20%. Crosses the blood–brain barrier and placenta.

MDElliottMD at 18:32, 14 May 2026

2026-05-14T18:32:14Z

← Older revision		Revision as of 18:32, 14 May 2026
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	\| starting_dose = 2.5 mg IR, 5 mg XR, or 12.5mg Mydayis		\| starting_dose = 2.5 mg IR, 5 mg XR, or 12.5mg Mydayis
	\| preparations = IR tabs 5, 7.5, 10, 12.5, 15, 20, 30 mg; XR caps 5, 10, 15, 20, 25, 30 mg; Mydayis caps 12.5, 25, 37.5, 50 mg		\| preparations = IR tabs 5, 7.5, 10, 12.5, 15, 20, 30 mg; XR caps 5, 10, 15, 20, 25, 30 mg; Mydayis caps 12.5, 25, 37.5, 50 mg
	\| fda_max = XR = 40 or 60 mg/d; IR = 40 or 60 mg/d<ref name="carlat/>		\| fda_max = XR = 40 or 60 mg/d; IR = 40 or 60 mg/d<ref name="carlat">https://www.thecarlatreport.com/articles/4464-stimulant-dosing-limits</ref>
	\| routes = Oral		\| routes = Oral
	\| onset = IR: 30–60 min; XR: 1–2 h to peak effect		\| onset = IR: 30–60 min; XR: 1–2 h to peak effect

MDElliottMD at 18:26, 14 May 2026

2026-05-14T18:26:48Z

← Older revision		Revision as of 18:26, 14 May 2026
Line 7:		Line 7:
	\| starting_dose = 2.5 mg IR, 5 mg XR, or 12.5mg Mydayis		\| starting_dose = 2.5 mg IR, 5 mg XR, or 12.5mg Mydayis
	\| preparations = IR tabs 5, 7.5, 10, 12.5, 15, 20, 30 mg; XR caps 5, 10, 15, 20, 25, 30 mg; Mydayis caps 12.5, 25, 37.5, 50 mg		\| preparations = IR tabs 5, 7.5, 10, 12.5, 15, 20, 30 mg; XR caps 5, 10, 15, 20, 25, 30 mg; Mydayis caps 12.5, 25, 37.5, 50 mg
	\| fda_max = ~~<ref name="carlat>~~XR = 40 or 60 mg/d; IR = 40 or 60 mg/d</~~ref~~>		\| fda_max = XR = 40 or 60 mg/d; IR = 40 or 60 mg/d<ref name="carlat/>
	\| routes = Oral		\| routes = Oral
	\| onset = IR: 30–60 min; XR: 1–2 h to peak effect		\| onset = IR: 30–60 min; XR: 1–2 h to peak effect

MDElliottMD at 18:26, 14 May 2026

2026-05-14T18:26:25Z

← Older revision		Revision as of 18:26, 14 May 2026
Line 7:		Line 7:
	\| starting_dose = 2.5 mg IR, 5 mg XR, or 12.5mg Mydayis		\| starting_dose = 2.5 mg IR, 5 mg XR, or 12.5mg Mydayis
	\| preparations = IR tabs 5, 7.5, 10, 12.5, 15, 20, 30 mg; XR caps 5, 10, 15, 20, 25, 30 mg; Mydayis caps 12.5, 25, 37.5, 50 mg		\| preparations = IR tabs 5, 7.5, 10, 12.5, 15, 20, 30 mg; XR caps 5, 10, 15, 20, 25, 30 mg; Mydayis caps 12.5, 25, 37.5, 50 mg
	\| fda_max =		\| fda_max = <ref name="carlat>XR = 40 or 60 mg/d; IR = 40 or 60 mg/d</ref>
	\| routes = Oral		\| routes = Oral
	\| onset = IR: 30–60 min; XR: 1–2 h to peak effect		\| onset = IR: 30–60 min; XR: 1–2 h to peak effect

← Older revision		Revision as of 03:16, 19 May 2026
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	\| pregnancy = Category C		\| pregnancy = Category C
	\| legal = Schedule II		\| legal = Schedule II
	\| mechanism = TAAR1 agonism, VMAT2 substrate, DAT/NET reverse transport — net release of dopamine and norepinephrine		\| mechanism = TAAR1 agonism, VMAT2 substrate, DAT/NET reverse transport, net release of dopamine and norepinephrine
	\| 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).		\| 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 med in the late 1920s. "Adderall" was approved by the FDA in 1996, and has since become one of the most popular meds in the United States. Adderall/MAS is FDA-approved for attention-deficit hyperactivity disorder and narcolepsy. It is listed in Schedule II of the Controlled Substances Act, and so is tightly regulated in the United States as well as many other countries around the world.		Amphetamine was first synthesized in 1887 by Lazăr Edeleanu, then developed as a med in the late 1920s. "Adderall" was approved by the FDA in 1996, and has since become one of the most popular meds in the United States. Adderall/MAS is FDA-approved for attention-deficit hyperactivity disorder and narcolepsy. It is listed in Schedule II of the Controlled Substances Act, and so is tightly regulated in the United States as well as many other countries around the world.
	\| indications = <problem ref="adhd" author="MDElliottMD"/>		\| indications = <problem ref="adhd" author="MDElliottMD"/>
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	Start at 5 mg XR; may increase by 5 mg each day until the desired effect is reached, up to 30 mg XR to start, and up to 60 mg XR eventually if necessary, in 10 mg increments.		Start at 5 mg XR; may increase by 5 mg each day until the desired effect is reached, up to 30 mg XR to start, and up to 60 mg XR eventually if necessary, in 10 mg increments.

	Occasionally can go higher if no notable effects (good or bad) at 60 mg — proceed with caution.		Occasionally can go higher if no notable effects (good or bad) at 60 mg, proceed with caution.

	If not long enough acting: add a tail dose of Adderall IR at [XR dose]/2.		If not long enough acting: add a tail dose of Adderall IR at [XR dose]/2.
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	<effect ref="executive-functioning"/>		<effect ref="executive-functioning"/>
	\| pk_absorption = Excellent oral bioavailability — sources report ">75%" to "~90%". Food does not significantly affect total absorption but can delay peak concentration.		\| pk_absorption = Excellent oral bioavailability, sources report ">75%" to "~90%". Food does not significantly affect total absorption but can delay peak concentration.
	\| pk_distribution = Volume of distribution ~4 L/kg; plasma protein binding less than 20%. Crosses the blood–brain barrier and placenta.		\| pk_distribution = Volume of distribution ~4 L/kg; plasma protein binding less than 20%. Crosses the blood–brain barrier and placenta.
	\| pk_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>S1</ref>		\| pk_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>S1</ref>
	\| pk_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:''' D-enantiomer 9 h (children 6–12 y), 11 h (adolescents 13–17 y), 10 h (adults); L-enantiomer 11 h, 13–14 h, 13 h respectively.		\| pk_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:''' D-enantiomer 9 h (children 6–12 y), 11 h (adolescents 13–17 y), 10 h (adults); L-enantiomer 11 h, 13–14 h, 13 h respectively.
	\| pharmacodynamics = Amphetamine purportedly works via several converging mechanisms at monoaminergic terminals:		\| pharmacodynamics = Amphetamine purportedly works via 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.		* '''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.		* '''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.'''		* '''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).		* '''Weak reuptake inhibition''' at DAT and NET (secondary to release).
	* '''MAO inhibition''' at higher concentrations, slowing presynaptic catabolism of monoamines.		* '''MAO inhibition''' at higher concentrations, slowing presynaptic catabolism of monoamines.
	* '''Serotonergic effects''' at high or supratherapeutic doses (relevant to overdose and serotonin syndrome risk).		* '''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.		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 = Minimal in practice. Caution with other psychostimulants, including caffeine. metabolized by 2D6, so relevant caution applies.		\| interactions = Minimal in practice. Caution with other psychostimulants, including caffeine. metabolized by 2D6, so relevant caution applies.
	<pharmaInteractions/>		<pharmaInteractions/>
	\| pregnancy_details = [https://www.ncbi.nlm.nih.gov/books/NBK501307/ 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.		\| pregnancy_details = [https://www.ncbi.nlm.nih.gov/books/NBK501307/ 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, weight/height, mental health history (especially for psychosis/bipolar/substance use risk), (optional) blood pressure, (optional) heart rate,		\| monitoring = * Baseline: cardiovascular history, weight/height, mental health history (especially for psychosis/bipolar/substance use risk), (optional) blood pressure, (optional) heart rate,
	* At each visit: efficacy, side effects, general well-being		* At each visit: efficacy, side effects, general well-being
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	* Sleep quality (insomnia is dose-limiting)		* Sleep quality (insomnia is dose-limiting)
	\| counseling = * Take first thing in the morning to minimize insomnia; avoid (late) afternoon dosing.		\| counseling = * Take first thing in the morning to minimize insomnia; avoid (late) 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.)		* '''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.		* Take with or without food; high-acid beverages (orange juice, vitamin C) may reduce absorption.
	* Stay well-hydrated, especially in heat or during exercise.		* Stay well-hydrated, especially in heat or during exercise.
	* Eat regular meals despite appetite suppression.		* Eat regular meals despite appetite suppression.
	* Report any chest pain, palpitations, severe agitation, hallucinations, or signs of poor circulation in extremities.		* Report any chest pain, palpitations, severe agitation, hallucinations, or signs of poor circulation in extremities.
	* Sudden discontinuation can cause a fatigue/depression "crash" — plan for it.		* Sudden discontinuation can cause a fatigue/depression "crash", plan for it.
	* Take caution: make increase bowel motility and increase risk of expelled fecal content.		* Take caution: make increase bowel motility and increase risk of expelled fecal content.
	\| anecdotes =		\| anecdotes =

← Older revision		Revision as of 02:30, 16 May 2026
Line 7:		Line 7:
	\| starting_dose = 2.5 mg IR, 5 mg XR, or 12.5mg Mydayis		\| starting_dose = 2.5 mg IR, 5 mg XR, or 12.5mg Mydayis
	\| preparations = IR tabs 5, 7.5, 10, 12.5, 15, 20, 30 mg; XR caps 5, 10, 15, 20, 25, 30 mg; Mydayis caps 12.5, 25, 37.5, 50 mg		\| preparations = IR tabs 5, 7.5, 10, 12.5, 15, 20, 30 mg; XR caps 5, 10, 15, 20, 25, 30 mg; Mydayis caps 12.5, 25, 37.5, 50 mg
	\| fda_max = XR = 40 or 60 mg/d; IR = 40 or 60 mg/d<ref name="carlat">~~https://www.thecarlatreport.com/articles/4464-stimulant-dosing-limits~~</ref>		\| fda_max = XR = 40 or 60 mg/d; IR = 40 or 60 mg/d<ref name="carlat">S0</ref>
	\| routes = Oral		\| routes = Oral
	\| onset = IR: 30–60 min; XR: 1–2 h to peak effect		\| onset = IR: 30–60 min; XR: 1–2 h to peak effect
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	\| pk_absorption = Excellent oral bioavailability — sources report ">75%" to "~90%". Food does not significantly affect total absorption but can delay peak concentration.		\| pk_absorption = Excellent oral bioavailability — sources report ">75%" to "~90%". Food does not significantly affect total absorption but can delay peak concentration.
	\| pk_distribution = Volume of distribution ~4 L/kg; plasma protein binding less than 20%. Crosses the blood–brain barrier and placenta.		\| pk_distribution = Volume of distribution ~4 L/kg; plasma protein binding less than 20%. Crosses the blood–brain barrier and placenta.
	\| pk_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>		\| pk_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>S1</ref>
	\| pk_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:''' D-enantiomer 9 h (children 6–12 y), 11 h (adolescents 13–17 y), 10 h (adults); L-enantiomer 11 h, 13–14 h, 13 h respectively.		\| pk_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:''' D-enantiomer 9 h (children 6–12 y), 11 h (adolescents 13–17 y), 10 h (adults); L-enantiomer 11 h, 13–14 h, 13 h respectively.
	\| pharmacodynamics = Amphetamine purportedly works via several converging mechanisms at monoaminergic terminals:		\| pharmacodynamics = Amphetamine purportedly works via several converging mechanisms at monoaminergic terminals:
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	\| monitoring = * Baseline: cardiovascular history, weight/height, mental health history (especially for psychosis/bipolar/substance use risk), (optional) blood pressure, (optional) heart rate,		\| monitoring = * Baseline: cardiovascular history, weight/height, mental health history (especially for psychosis/bipolar/substance use risk), (optional) blood pressure, (optional) heart rate,
	* At each visit: efficacy, side effects, general well-being		* At each visit: efficacy, side effects, general well-being
	* Periodically reassess continued need; consider ~~drug~~ holidays to assess ongoing benefit		* Periodically reassess continued need; consider medicine holidays to assess ongoing benefit
	* Sleep quality (insomnia is dose-limiting)		* Sleep quality (insomnia is dose-limiting)
	\| counseling = * Take first thing in the morning to minimize insomnia; avoid (late) afternoon dosing.		\| counseling = * Take first thing in the morning to minimize insomnia; avoid (late) afternoon dosing.