RESEARCH MONOGRAPH · KDC-MN-380

Dextroamphetamine

May 9, 2026 Kodiac biolabs Research Revised May 30, 2026 2 min read

Our opinion on this compound

75/100

The dopaminergic-preferring amphetamine enantiomer; cleaner pharmacology than the racemate for receptor work

D-amphetamine is the dopaminergic-preferring enantiomer, roughly 3 to 4x more potent than l-amphetamine at the dopamine transporter while being only modestly more potent at NET. So if you want amphetamine pharmacology with a relatively cleaner dopamine signal, this is your tool compound. The racemate (Adderall) is a 3:1 d:l salt mixture, which means it intentionally adds noradrenergic tone for the ADHD indication. Pure d-amphetamine (Dexedrine, Zenzedi) sits closer to the dopamine-mediated effects.

The history is interesting and underappreciated. D-amphetamine sulfate was one of the first prescribed psychiatric medications in the 1930s under the trade name Dexedrine. Smith Kline ran it for narcolepsy, depression, obesity, and what was then called minimal brain dysfunction. The narcolepsy and ADHD indications survived. The depression and obesity uses didn't, mostly for tolerance and abuse-liability reasons that are well documented.

What we like for research applications: head-to-head with l-amphetamine or with selective NRIs, you can dissect dopamine vs noradrenergic contributions to specific behaviors. The d-isomer's preference for VMAT-mediated cytosolic accumulation is also slightly different from the l-isomer, which matters for vesicular release kinetics work.

What people miss is the clinical preference data. A subset of ADHD patients respond noticeably better to pure d-amphetamine than to mixed amphetamine salts. Probably reflects individual variation in NET versus DAT contribution to symptom relief. There's a small but real prescribing community that uses Zenzedi specifically for that reason.

Sourcing is the same regulatory situation as amphetamine, Schedule II, pharmaceutical-grade reference standards available with licensing, and the enantiomeric purity is the critical QC parameter. Chiral HPLC or polarimetry should show 99 plus ee. Anything less means residual l-isomer contamination, which confounds receptor selectivity work.

Stability is fine in the sulfate salt form, the freebase is volatile and oxidizes, so most material is sold and stored as sulfate or saccharate.

Staying power is high. It's the reference compound for dopaminergic releaser pharmacology and that's not going to change.

Evidence: 88
Mechanism: 92
Reliability: 85
Safety: 55
Sourcing: 60
Value: 60
Signal: 78
Staying power: 85

Plain-language summary Intrigue 65 / 100

Dextroamphetamine is the d-enantiomer of amphetamine, sold as Dexedrine since 1976. The d-form is roughly two to three times more potent at central dopamine release than the l-form, while both release norepinephrine about equally. The practical result is a stimulant tilted toward CNS dopamine effects with somewhat less peripheral cardiovascular load than racemic mixtures like Adderall. Approved for ADHD and narcolepsy. Schedule II. Used clinically when patients tolerate racemic amphetamine poorly and as the canonical pure d-amphetamine reference in research where investigators need to isolate the dopaminergic component of the response. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

d-enantiomer amphetamine (dopaminergic-preferring)

The d-enantiomer of amphetamine; a more dopaminergic stimulant than the racemic mixture, used in ADHD and narcolepsy.

Abstract

Dextroamphetamine ((S)-1-phenylpropan-2-amine, d-amphetamine; CAS 51-64-9; molecular formula C9H13N; molecular weight 135.21) is the d-enantiomer of amphetamine, approved by the FDA in 1976 (Dexedrine). The d-enantiomer is approximately 2 to 3 fold more potent at central dopamine release than the l-enantiomer; both enantiomers have approximately equivalent norepinephrine release. The pharmacology versus racemic amphetamine is shifted toward CNS dopaminergic effects with reduced peripheral cardiovascular activity. Approved indications: ADHD, narcolepsy. Plasma half-life is approximately 12 hours. Schedule II. Used as the canonical pure d-amphetamine in research and clinical practice for patients tolerating racemic amphetamine poorly.

Mechanism of action

d-enantiomer of amphetamine; ~2-3 fold more potent at dopamine release than l-enantiomer. Same monoamine releaser mechanism with shifted CNS:peripheral profile.

Reported research dose ranges

Clinical 5 to 60 mg in the published literature.

References

Heal DJ, et al. Amphetamine, past and present. J Psychopharmacol 2013.
Easton N, et al. The dopaminergic basis of behavioral and pharmacological actions of d-amphetamine. Eur Neuropsychopharmacol 2007.
Wilens TE. Effects of methylphenidate on the catecholaminergic system in attention-deficit/hyperactivity disorder. J Clin Psychopharmacol 2008.

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KDC-MN-380

The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.

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Dextroamphetamine

Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

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Abstract

Mechanism of action

Reported research dose ranges

References

Read the full monograph

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